KINDAI UNIVERSITY


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MORIYAMA Hiroyuki

Profile

FacultyPharmaceutical Research and Technology Institute
PositionAssociate Professor
Degree
Commentator Guidehttps://www.kindai.ac.jp/meikan/665-moriyama-hiroyuki.html
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Last Updated :2020/09/30

Education and Career

Academic & Professional Experience

  •   2014 , 准教授, 近畿大学

Research Activities

Research Areas

  • Life sciences, Dermatology
  • Life sciences, Cell biology

Published Papers

  • Notch Signaling Enhances Stemness by Regulating Metabolic Pathways Through Modifying p53, NF-κB, and HIF-1α., Hiroyuki Moriyama, Mariko Moriyama, Toshiyuki Ozawa, Daisuke Tsuruta, Taro Iguchi, Satoshi Tamada, Tatsuya Nakatani, Koichi Nakagawa, Takao Hayakawa, Stem cells and development, Stem cells and development, 27(13), 935 - 947, Jul. 01 2018 , Refereed
    Summary:Human adipose-derived mesenchymal stromal cells (hASCs) are attractive for regenerative medicine, but their limited in vitro life span limits their therapeutic applicability. Recent data demonstrate that hypoxia may benefit the ex vivo culture of stem cells. Such cells exhibit a high level of glycolytic metabolism under hypoxic conditions. However, the physiological role of glycolytic activation and its underlying regulatory mechanism are incompletely understood. We have shown that when activated under conditions of 5% O2, Notch signaling dramatically increases the rate of glycolysis, improves proliferation efficiency, prevents senescence, and maintains the multipotency of hASCs. In the present study, we found that activated Notch1 enhanced nuclear p65 levels, resulting in an increase in glucose metabolism through the upregulation of glycolytic factors, including GLUT3. Notch signaling was also involved in glucose metabolism through p53 inactivation. We also found that NF-κB signaling was regulated by p53. These data suggest that Notch-HES1 signaling enhances the glycolytic pathway through p53 and NF-κB. Our data also revealed that activated Notch1 markedly increased the transcriptional activity of hypoxia-inducible factor 1 (HIF-1). Knockdown of HIF-1α significantly attenuated glycolysis induced by activated Notch1, indicating that the glycolysis pathway is regulated by the coordination of Notch signaling and HIF. Overall, our observations provide new regulatory mechanisms for the glycolysis by Notch signaling to maintain the stemness of hASCs.
  • Identification of ACA-28, a 1'-acetoxychavicol acetate analogue compound, as a novel modulator of ERK MAPK signaling, which preferentially kills human melanoma cells., Satoh Ryosuke, Hagihara Kanako, Matsuura Kazuki, Manse Yoshiaki, Kita Ayako, Kunoh Tatsuki, Masuko Takashi, Moriyama Mariko, Moriyama Hiroyuki, Tanabe Genzoh, Muraoka Osamu, Sugiura Reiko, Genes to cells : devoted to molecular & cellular mechanisms, Genes to cells : devoted to molecular & cellular mechanisms, 22(7), 608-618, Jul. 2017 , Refereed
    Summary:Here, we carried out a chemical genetic screen using a fission yeast phenotypic assay and showed that ACA-28, a synthetic derivative of 1'-acetoxychavicol acetate (ACA), which is a natural ginger compound, effectively inhibited the growth of melanoma cancer cells wherein ERK MAPK signaling is hyperactivated due to mutations in the upstream activating regulators. ACA-28 more potently inhibited the growth of melanoma cells than did the parental compound ACA. Importantly, the growth of normal human epidermal melanocytes (NHEM) was less affected by ACA-28 at the same 50% inhibitory concentration. In addition, ACA-28 specifically induced apoptosis in NIH/3T3 cells which were oncogenically transformed with human epidermal growth factor receptor-2 (HER2/ErbB2), but not in the parental cells. ACA-28 might serve as a promising seed compound for melanoma treatment.
  • Antenatal corticosteroids and preterm offspring outcomes in hypertensive disorders of pregnancy: A Japanese cohort study., Takafumi Ushida, Tomomi Kotani, Masahiro Hayakawa, Akihiro Hirakawa, Ryo Sadachi, Noriyuki Nakamura, Yoshinori Moriyama, Kenji Imai, Tomoko Nakano-Kobayashi, Fumitaka Kikkawa, Scientific reports, Scientific reports, 10(1), 9312 - 9312, Jun. 09 2020 , Refereed
    Summary:To estimate whether antenatal corticosteroids (ACS) improve short- and long-term preterm offspring outcomes in singleton pregnancies complicated by hypertensive disorders of pregnancy (HDP) similar to pregnancies without HDP. This population-based retrospective study was conducted based on an analysis of data collected by the Neonatal Research Network of Japan on 21,014 singleton neonates weighing ≤1,500 g between 24 and 31 weeks' gestation during 2003-2016. Logistic regression analyses were performed to compare short- and long-term offspring outcomes between mothers receiving ACS treatment and those who did not among pregnancies with HDP and without HDP. Of 21,014 neonates, 4,806 (22.9%) were born to mothers with HDP. ACS treatment was associated with significant decreases in short-term adverse outcomes in the both HDP and non-HDP groups, with similar reduced odds of neonatal death, respiratory distress syndrome, and intraventricular haemorrhage (IVH). However, ACS treatment did not significantly decrease severe IVH (aOR 0.76; 95% CI 0.51-1.13) and periventricular leukomalacia (1.14; 0.78-1.66) in the HDP group. In addition, ACS treatment in mothers without HDP significantly decreased cerebral palsy (aOR 0.70; 95% CI 0.58-084), developmental quotient scores <85 (0.79; 0.69-0.90), and composite adverse outcomes (0.85; 0.75-0.96) at 3 years of age, whereas ACS treatment in mothers with HDP did not significantly improve these outcomes (1.04; 0.69-1.57, 1.11; 0.88-1.39, 0.96; 0.75-1.22, respectively). ACS treatment was associated with significantly decreased major short-term morbidities and mortality among extremely and very preterm neonates of mothers with HDP, with ACS treatment having a decreased effect compared to that observed in neonates of mothers without HDP. Although ACS treatment has no additional effects on offspring outcomes at 3 years of age, our results did not suggest that ACS treatment should be withheld from mothers with HDP.
  • Exploration of the Pressurization Condition for Killing Human Skin Cells and Skin Tumor Cells by High Hydrostatic Pressure., Toshihito Mitsui, Naoki Morimoto, Atsushi Mahara, Sharon Claudia Notodihardjo, Tien Minh Le, Maria Chiara Munisso, Mariko Moriyama, Hiroyuki Moriyama, Natsuko Kakudo, Tetsuji Yamaoka, Kenji Kusumoto, BioMed research international, BioMed research international, 2020, 9478789 - 9478789, 2020 , Refereed
    Summary:High hydrostatic pressure (HHP) is a physical method for inactivating cells or tissues without using chemicals such as detergents. We previously reported that HHP at 200 MPa for 10 min was able to inactivate all cells in skin and giant congenital melanocytic nevus (GCMN) without damaging the extracellular matrix. We also reported that HHP at 150 MPa for 10 min was not sufficient to inactivate them completely, while HHP at 200 MPa for 10 min was able to inactivate them completely. We intend to apply HHP to treat malignant skin tumor as the next step; however, the conditions necessary to kill each kind of cell have not been explored. In this work, we have performed a detailed experimental study on the critical pressure and pressurization time using five kinds of human skin cells and skin tumor cells, including keratinocytes (HEKas), dermal fibroblasts (HDFas), adipose tissue-derived stem cells (ASCs), epidermal melanocytes (HEMa-LPs), and malignant melanoma cells (MMs), using pressures between 150 and 200 MPa. We pressurized cells at 150, 160, 170, 180, or 190 MPa for 1 s, 2 min, and 10 min and evaluated the cellular activity using live/dead staining and proliferation assays. The proliferation assay revealed that HEKas were inactivated at a pressure higher than 150 MPa and a time period longer than 2 min, HDFas and MMs were inactivated at a pressure higher than 160 MPa and for 10 min, and ASCs and HEMa-LPs were inactivated at a pressure higher than 150 MPa and for 10 min. However, some HEMa-LPs were observed alive after HHP at 170 MPa for 10 min, so we concluded that HHP at a pressure higher than 180 MPa for 10 min was able to inactivate five kinds of cells completely.
  • Adipose-derived stromal/stem cells improve epidermal homeostasis., Mariko Moriyama, Shunya Sahara, Kaori Zaiki, Ayumi Ueno, Koichi Nakaoji, Kazuhiko Hamada, Toshiyuki Ozawa, Daisuke Tsuruta, Takao Hayakawa, Hiroyuki Moriyama, Scientific reports, Scientific reports, 9(1), 18371 - 18371, Dec. 04 2019 , Refereed
    Summary:Wound healing is regulated by complex interactions between the keratinocytes and other cell types including fibroblasts. Recently, adipose-derived mesenchymal stromal/stem cells (ASCs) have been reported to influence wound healing positively via paracrine involvement. However, their roles in keratinocytes are still obscure. Therefore, investigation of the precise effects of ASCs on keratinocytes in an in vitro culture system is required. Our recent data indicate that the epidermal equivalents became thicker on a collagen vitrigel membrane co-cultured with human ASCs (hASCs). Co-culturing the human primary epidermal keratinocytes (HPEK) with hASCs on a collagen vitrigel membrane enhanced their abilities for cell proliferation and adhesion to the membrane but suppressed their differentiation suggesting that hASCs could maintain the undifferentiated status of HPEK. Contrarily, the effects of co-culture using polyethylene terephthalate or polycarbonate membranes for HPEK were completely opposite. These differences may depend on the protein permeability and/or structure of the membrane. Taken together, our data demonstrate that hASCs could be used as a substitute for fibroblasts in skin wound repair, aesthetic medicine, or tissue engineering. It is also important to note that a co-culture system using the collagen vitrigel membrane allows better understanding of the interactions between the keratinocytes and ASCs.
  • Role of FBXW7 in the quiescence of gefitinib-resistant lung cancer stem cells in EGFR-mutant non-small cell lung cancer., Moulid Hidayat, Yoichiro Mitsuishi, Fumiyuki Takahashi, Ken Tajima, Toshifumi Yae, Katsumi Miyahara, Daisuke Hayakawa, Wira Winardi, Hiroaki Ihara, Yoshika Koinuma, Aditya Wirawan, Fariz Nurwidya, Motoyasu Kato, Isao Kobayashi, Shinichi Sasaki, Kazuya Takamochi, Takuo Hayashi, Yoshiyuki Suehara, Mariko Moriyama, Hiroyuki Moriyama, Sonoko Habu, Kazuhisa Takahashi, Bosnian journal of basic medical sciences, Bosnian journal of basic medical sciences, 19(4), 355 - 367, Nov. 08 2019 , Refereed
    Summary:Several recent studies suggest that cancer stem cells (CSCs) are involved in intrinsic resistance to cancer treatment. Maintenance of quiescence is crucial for establishing resistance of CSCs to cancer therapeutics. F-box/WD repeat-containing protein 7 (FBXW7) is a ubiquitin ligase that regulates quiescence by targeting the c-MYC protein for ubiquitination. We previously reported that gefitinib-resistant persisters (GRPs) in EGFR-mutant non-small cell lung cancer (NSCLC) cells highly expressed octamer-binding transcription factor 4 (Oct-4) as well as the lung CSC marker CD133, and they exhibited distinctive features of the CSC phenotype. However, the role of FBXW7 in lung CSCs and their resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors in NSCLC is not fully understood. In this study, we developed GRPs from the two NSCLC cell lines PC9 and HCC827, which express an EGFR exon 19 deletion mutation, by treatment with a high concentration of gefitinib. The GRPs from both PC9 and HCC827 cells expressed high levels of CD133 and FBXW7, but low levels of c-MYC. Cell cycle analysis demonstrated that the majority of GRPs existed in the G0/G1 phase. Knockdown of the FBXW7 gene significantly reduced the cell number of CD133-positive GRPs and reversed the cell population in the G0/G1-phase. We also found that FBXW7 expression in CD133-positive cells was increased and c-MYC expression was decreased in gefitinib-resistant tumors of PC9 cells in mice and in 9 out of 14 tumor specimens from EGFR-mutant NSCLC patients with acquired resistance to gefitinib. These findings suggest that FBXW7 plays a pivotal role in the maintenance of quiescence in gefitinib-resistant lung CSCs in EGFR mutation-positive NSCLC.
  • C-reactive protein can be used to predict the therapeutic effects of nivolumab in patients with metastatic renal cell carcinoma., Jun Teishima, Daiki Murata, Yasuhisa Hasegawa, Hiroyuki Moriyama, Koji Mita, Akio Matsubara, International journal of urology : official journal of the Japanese Urological Association, International journal of urology : official journal of the Japanese Urological Association, 26(11), 1076 - 1077, Nov. 2019 , Refereed
  • Somatic symptom disorder manifested as acute abdominal pain during pregnancy preceding perinatal depression: a case report, Yoshinori Moriyama, Kenji Imai, Tomoko Nakano, Tomomi Kotani, Fumitaka Kikkawa, Archives of Women's Mental Health, Archives of Women's Mental Health, 1 - 4, May 26 2018 , Refereed
    Summary:Somatic symptom disorder (SSD) occurring as abdominal pain during pregnancy can be very difficult to distinguish from physical diseases prompt diagnosis and appropriate treatment are required. SSD can develop into perinatal depression, which may need intensive psychiatric intervention. Here, we present the first case report of SSD preceding perinatal depression. This case shows the clinical importance of SSD in obstetrics both as a cause of abdominal pain and as a precursor of depression.
  • The effect of kinetics of C-reactive protein in the prediction of overall survival in patients with metastatic renal cell carcinoma treated with tyrosine kinase inhibitor, Jun Teishima, Kohei Kobatake, Shunsuke Shinmei, Shogo Inoue, Tetsutaro Hayashi, Shinya Ohara, Koji Mita, Yasuhisa Hasegawa, Satoshi Maruyama, Mitsuru Kajiwara, Masanobu Shigeta, Hideki Mochizuki, Hiroyuki Moriyama, Seiji Fujiwara, Akio Matsubara, UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS, UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS, 35(11), Nov. 2017 , Refereed
    Summary:Introduction and objectives: The aim of this study was to investigate the effect of kinetics of C-reactive protein (CRP) in the prediction of overall survival (OS) in patients with metastatic renal cell carcinoma (mRCC) treated with a tyrosine kinase inhibitor. Materials and methods: The CRP in 118 cases of molecular-targeted therapy for mRCC was measured before starting the prescription of the first-line targeted agents and at the first time a CT scan was conducted during treatments. All cases were classified into higher-CRP groups and lower ones according to their data at the time of starting treatments. A higher-CRP group was further classified into 2 subgroups based on the kinetics after first-line targeted therapy: "decreased-CRP subgroup" and "nondecreased CRP subgroup." Results: The median of the observation period was 23.4 months. The OS in cases with CRP higher than 0.5 mg/dl was significantly worse than those in other cases (P < 0.0001). Multivariate analysis revealed that the pretreated CRP (hazard ratio = 2.093; 95% CI: 1.176-3.858; P = 0.0179) was an independent predictive factor of OS. In the higher-CRP group, the OS for the decreased-CRP subgroup (1 year, 85.0%) was significantly better than those for the nondecreased CRP subgroup (1 year, 37.2%, P < 0.0001). Multivariate analyses in the higher-CRP group revealed that the decrease in the CRP was an independent predictive factor for OS (hazard ratio = 0.176; 95% CI: 0.064-0.488; P = 0.0008). Conclusion: A decrease in CRP as well as pretreatment CRP can be a predictive factor for OS in patients with mRCC treated with a tyrosine kinase inhibitor. Cases with mRCC could be stratified into 3 groups with different prognoses using the pretreated CRP and its changes. (C) 2017 Elsevier Inc. All rights reserved.
  • Identification of ACA-28, a 1'-acetoxychavicol acetate analogue compound, as a novel modulator of ERK MAPK signaling, which preferentially kills human melanoma cells., Ryosuke Satoh, Kanako Hagihara, Kazuki Matsuura, Yoshiaki Manse, Ayako Kita, Tatsuki Kunoh, Takashi Masuko, Mariko Moriyama, Hiroyuki Moriyama, Genzoh Tanabe, Osamu Muraoka, Reiko Sugiura, Genes to cells : devoted to molecular & cellular mechanisms, Genes to cells : devoted to molecular & cellular mechanisms, 22(7), 608 - 618, Jul. 2017 , Refereed
    Summary:The extracellular signal-regulated kinase (ERK) signaling pathway is essential for cell proliferation and is frequently deregulated in human tumors such as melanoma. Melanoma remains incurable despite the use of conventional chemotherapy; consequently, development of new therapeutic agents for melanoma is highly desirable. Here, we carried out a chemical genetic screen using a fission yeast phenotypic assay and showed that ACA-28, a synthetic derivative of 1'-acetoxychavicol acetate (ACA), which is a natural ginger compound, effectively inhibited the growth of melanoma cancer cells wherein ERK MAPK signaling is hyperactivated due to mutations in the upstream activating regulators. ACA-28 more potently inhibited the growth of melanoma cells than did the parental compound ACA. Importantly, the growth of normal human epidermal melanocytes (NHEM) was less affected by ACA-28 at the same 50% inhibitory concentration. In addition, ACA-28 specifically induced apoptosis in NIH/3T3 cells which were oncogenically transformed with human epidermal growth factor receptor-2 (HER2/ErbB2), but not in the parental cells. Notably, the ACA-28-induced apoptosis in melanoma and HER2-transformed cells was abrogated when ERK activation was blocked with a specific MEK inhibitor U0126. Consistently, ACA-28 more strongly stimulated ERK phosphorylation in melanoma cells, as compared in NHEM. ACA-28 might serve as a promising seed compound for melanoma treatment.
  • BNIP3 upregulation via stimulation of ERK and JNK activity is required for the protection of keratinocytes from UVB-induced apoptosis., Mariko Moriyama, Hiroyuki Moriyama, Junki Uda, Hirokazu Kubo, Yuka Nakajima, Arisa Goto, Takashi Morita, Takao Hayakawa, Cell death & disease, Cell death & disease, 8(2), e2576 - 200, Feb. 02 2017 , Refereed
    Summary:The human skin has an important role in barrier function. Ultraviolet rays (UV) from sunlight exposure can cause cell apoptosis in the skin epidermis, resulting in the disruption of the barrier. Previously, we have demonstrated that BNIP3 stimulates autophagy in epidermal keratinocytes and has a protective effect in these cells upon UVB irradiation. In this study, we found that the accumulation of reactive oxygen species (ROS) by UVB irradiation was sufficient to trigger the activation of JNK and ERK mitogen-activated protein kinase (MAPK) in human primary epidermal keratinocytes. In turn, activated JNK and ERK MAPK mediated the upregulation of BNIP3 expression. Treatment with an antioxidant reagent or a specific inhibitor of MAPK, U0126, and a JNK inhibitor significantly attenuated the expression of BNIP3 triggered by UVB, followed by the induction of cell death by apoptosis. Furthermore, UVB-induced apoptosis was significantly stimulated by chloroquine or bafilomycin A1, an inhibitor of autophagy. Moreover, BNIP3 was required for the degradation of dysfunctional mitochondria upon UVB irradiation. These data clearly indicated that BNIP3-induced autophagy, which occurs via UVB-generated ROS-mediated JNK and ERK MAPK activation, has a crucial role in the protection of the skin epidermis against UVB irradiation.
  • Oct4 plays a crucial role in the maintenance of gefitinib-resistant lung cancer stem cells., Isao Kobayashi, Fumiyuki Takahashi, Fariz Nurwidya, Takeshi Nara, Muneaki Hashimoto, Akiko Murakami, Shigehiro Yagishita, Ken Tajima, Moulid Hidayat, Naoko Shimada, Kentaro Suina, Yasuko Yoshioka, Shinichi Sasaki, Mariko Moriyama, Hiroyuki Moriyama, Kazuhisa Takahashi, Biochemical and biophysical research communications, Biochemical and biophysical research communications, 473(1), 125 - 132, Apr. 22 2016 , Refereed
    Summary:Several recent studies have suggested that cancer stem cells (CSCs) are involved in resistance to gefitinib in non-small cell lung cancer (NSCLC). Oct4, a member of the POU-domain transcription factor family, has been shown to be involved in CSC properties of various cancers. We previously reported that Oct4 and the putative lung CSC marker CD133 were highly expressed in gefitinib-resistant persisters (GRPs) in NSCLC cells, and GRPs exhibited characteristic features of the CSCs phenotype. The aim of this study was to elucidate the role of Oct4 in the resistance to gefitinib in NSCLC cells with an activating epidermal growth factor receptor (EGFR) mutation. NSCLC cell lines, PC9, which express the EGFR exon 19 deletion mutation, were transplanted into NOG mice, and were treated with gefitinib in vivo. After 14-17 days of gefitinib treatment, the tumors still remained; these tumors were referred to as gefitinib-resistant tumors (GRTs). PC9-GRTs showed higher expression of Oct4 and CD133. To investigate the role of Oct4 in the maintenance of gefitinib-resistant lung CSCs, we introduced the Oct4 gene into PC9 and HCC827 cells carrying an activating EGFR mutation by lentiviral infection. Transfection of Oct4 significantly increased CD133-positive GRPs and the number of sphere formation, reflecting the self-renewal activity, of PC9 and HCC827 cells under the high concentration of gefitinib in vitro. Furthermore, Oct4-overexpressing PC9 cells (PC9-Oct4) significantly formed tumors at 1 × 10 cells/injection in NOG mice as compared to control cells. In addition, PC9-Oct4 tumors were more resistant to gefitinib treatment as compared to control cells in vivo. Finally, immunohistochemical analysis revealed that Oct4 was highly expressed in tumor specimens of EGFR-mutant NSCLC patients with acquired resistance to gefitinib. Collectively, these findings suggest that Oct4 plays a pivotal role in the maintenance of lung CSCs resistant to gefitinib in EGFR mutation-positive NSCLC.
  • Inhibitory Effects of Oligostilbenoids from the Bark of Shorea roxburghii on Malignant Melanoma Cell Growth: Implications for Novel Topical Anticancer Candidates., Hiroyuki Moriyama, Mariko Moriyama, Kiyofumi Ninomiya, Toshio Morikawa, Takao Hayakawa, Biological & pharmaceutical bulletin, Biological & pharmaceutical bulletin, 39(10), 1675 - 1682, 2016 , Refereed
    Summary:Human malignant melanomas remain associated with dismal prognosis due to their resistance to apoptosis and chemotherapy. There is growing interest in plant oligostilbenoids owing to their pleiotropic biological activities, including anti-inflammatory, antioxidant, and anticancer effects. Recent studies have demonstrated that resveratrol, a well-known stilbenoid from red wine, exhibits cell cycle-disrupting and apoptosis-inducing activities on melanoma cells. The objective of our study was to evaluate the anti-melanoma effect of oligostilbenoids isolated from the bark of Shorea roxburghii. Among the isolates, four resveratrol oligomers, i.e., (-)-hopeaphenol, vaticanol B, hemsleyanol D, and (+)-α-viniferin, possessed more potent antiproliferative action than did resveratrol against SK-MEL-28 melanoma cells. Cell cycle analysis revealed that (-)-hopeaphenol, hemsleyanol D, and (+)-α-viniferin arrested cell division cycle at the G1 phase, whereas vaticanol B had little effect on the cell cycle. In addition, cell proliferation assay also revealed that (+)-α-viniferin induced DNA damage followed by induction of apoptosis in SK-MEL-28 cells, which was confirmed by an increased expression of γ-H2AX and cleaved caspase-3, respectively. The compounds vaticanol B, hemsleyanol D, and resveratrol significantly increased the expression of p21, suggesting that they are able to block cell cycle progression. Moreover, these oligostilbenoids downmodulated cylin D1 expression and extracellular signal-regulated kinase (ERK) activation. Furthermore, hemsleyanol D, (+)-α-viniferin, and resveratrol significantly decreased the expression of cyclin B1, which could also suppress cell cycle progression. The present study thus suggests that these plant oligostilbenoids are effective as therapeutic or chemopreventive agents against melanoma.
  • Beneficial Effects of the Genus Aloe on Wound Healing, Cell Proliferation, and Differentiation of Epidermal Keratinocytes., Mariko Moriyama, Hiroyuki Moriyama, Junki Uda, Hirokazu Kubo, Yuka Nakajima, Arisa Goto, Junji Akaki, Ikuyo Yoshida, Nobuya Matsuoka, Takao Hayakawa, PloS one, PloS one, 11(10), e0164799, 2016 , Refereed
    Summary:Aloe has been used as a folk medicine because it has several important therapeutic properties. These include wound and burn healing, and Aloe is now used in a variety of commercially available topical medications for wound healing and skin care. However, its effects on epidermal keratinocytes remain largely unclear. Our data indicated that both Aloe vera gel (AVG) and Cape aloe extract (CAE) significantly improved wound healing in human primary epidermal keratinocytes (HPEKs) and a human skin equivalent model. In addition, flow cytometry analysis revealed that cell surface expressions of β1-, α6-, β4-integrin, and E-cadherin increased in HPEKs treated with AVG and CAE. These increases may contribute to cell migration and wound healing. Treatment with Aloe also resulted in significant changes in cell-cycle progression and in increases in cell number. Aloe increased gene expression of differentiation markers in HPEKs, suggesting roles for AVG and CAE in the improvement of keratinocyte function. Furthermore, human skin epidermal equivalents developed from HPEKs with medium containing Aloe were thicker than control equivalents, indicating the effectiveness of Aloe on enhancing epidermal development. Based on these results, both AVG and CAE have benefits in wound healing and in treatment of rough skin.
  • Lymphoepithelioma-like carcinoma of the urinary bladder: A case report and review of the literature, Tateki Yoshino, Shinya Ohara, Hiroyuki Moriyama, BMC Research Notes, BMC Research Notes, 7(1), Nov. 04 2014 , Refereed
    Summary:Background: Lymphoepithelioma-like carcinoma is an undifferentiated carcinoma with histological features similar to undifferentiated, non-keratinizing carcinoma of the nasopharynx. Lymphoepithelioma-like carcinoma of the urinary bladder is uncommon with a reported incidence of 0.3%- 1.3% of all bladder cancer. We report a Japanese case of predominant lymphoepithelioma-like carcinoma of the urinary bladder and review all of the English literature after performing a pooled analysis of the cases including the present one. Case presentation: An 83-year-old Japanese man was introduced to our department with the chief complaint of macroscopic hematuria. Cystoscopy demonstrated a thumb tip-sized bladder tumor at the trigone. The patient underwent a transurethral resection of the bladder tumor. The pathological examination showed predominant lymphoepithelioma-like carcinoma of the urinary bladder with urothelial carcinoma. The patient was diagnosed with muscle invasive lymphoepithelioma-like carcinoma of the urinary bladder and was treated with concurrent chemoradiotherapy. The patient is under observation with regular clinical follow-up and remains well after 12 months, with no evidence of disease recurrence. The reports of 93 patients including the present one of lymphoepithelioma-like carcinoma of the urinary bladder from the English literature were collected between 1991 and 2014. Patients were evaluated for clinicopathological findings. Outcome resulted as follows: 59 patients (67%) did not show evidence of disease, 14 (17%) died of disease, 5 (6%) was alive with metastases, and 9 (10%) died for causes unrelated to the primary disease. Cause-specific survival rate resulted 83%. The overall patients were divided into three groups (pure, predominant and focal) according to the lymphoepithelioma-like carcinoma of the urinary bladder classification of Amin et al. Conclusions: Because lymphoepithelioma-like carcinoma of the urinary bladder is more sensitive to both chemotherapy and radiotherapy than conventional urothelial carcinoma, radical cystectomy may not be necessary for all patients with muscle invasive lymphoepithelioma-like carcinoma of the urinary bladder. Therefore, pathological information may be useful in selecting patients suitable for bladder-preservation treatment. On the other hand, the apparently more aggressive nature of focal lymphoepithelioma-like carcinoma of the urinary bladder suggests that these patients are probably best managed with radical cystectomy and adjuvant treatment.
  • Role of notch signaling in the maintenance of human mesenchymal stem cells under hypoxic conditions., Hiroyuki Moriyama, Mariko Moriyama, Haruki Isshi, Shin Ishihara, Hanayuki Okura, Akihiro Ichinose, Toshiyuki Ozawa, Akifumi Matsuyama, Takao Hayakawa, Stem cells and development, Stem cells and development, 23(18), 2211 - 24, Sep. 15 2014 , Refereed
    Summary:Human adipose tissue-derived multilineage progenitor cells (hADMPCs) are attractive for cell therapy and tissue engineering because of their multipotency and ease of isolation without serial ethical issues. However, their limited in vitro lifespan in culture systems hinders their therapeutic application. Some somatic stem cells, including hADMPCs, are known to be localized in hypoxic regions; thus, hypoxia may be beneficial for ex vivo culture of these stem cells. These cells exhibit a high level of glycolytic metabolism in the presence of high oxygen levels and further increase their glycolysis rate under hypoxia. However, the physiological role of glycolytic activation and its regulatory mechanisms are still incompletely understood. Here, we show that Notch signaling is required for glycolysis regulation under hypoxic conditions. Our results demonstrate that 5% O2 dramatically increased the glycolysis rate, improved the proliferation efficiency, prevented senescence, and maintained the multipotency of hADMPCs. Intriguingly, these effects were not mediated by hypoxia-inducible factor (HIF), but rather by the Notch signaling pathway. Five percent O2 significantly increased the level of activated Notch1 and expression of its downstream gene, HES1. Furthermore, 5% O2 markedly increased glucose consumption and lactate production of hADMPCs, which decreased back to normoxic levels on treatment with a γ-secretase inhibitor. We also found that HES1 was involved in induction of GLUT3, TPI, and PGK1 in addition to reduction of TIGAR and SCO2 expression. These results clearly suggest that Notch signaling regulates glycolysis under hypoxic conditions and, thus, likely affects the cell lifespan via glycolysis.
  • BNIP3 plays crucial roles in the differentiation and maintenance of epidermal keratinocytes., Mariko Moriyama, Hiroyuki Moriyama, Junki Uda, Akifumi Matsuyama, Masatake Osawa, Takao Hayakawa, The Journal of investigative dermatology, The Journal of investigative dermatology, 134(6), 1627 - 1635, Jun. 2014 , Refereed
    Summary:Transcriptome analysis of the epidermis of Hes1(-/-) mouse revealed the direct relationship between Hes1 (hairy and enhancer of split-1) and BNIP3 (BCL2 and adenovirus E1B 19-kDa-interacting protein 3), a potent inducer of autophagy. Keratinocyte differentiation is going along with activation of lysosomal enzymes and organelle clearance, expecting the contribution of autophagy in this process. We found that BNIP3 was expressed in the suprabasal layer of the epidermis, where autophagosome formation is normally observed. Forced expression of BNIP3 in human primary epidermal keratinocytes (HPEKs) resulted in autophagy induction and keratinocyte differentiation, whereas knockdown of BNIP3 had the opposite effect. Intriguingly, addition of an autophagy inhibitor significantly suppressed the BNIP3-stimulated differentiation of keratinocytes, suggesting that BNIP3 plays a crucial role in keratinocyte differentiation by inducing autophagy. Furthermore, the number of dead cells increased in the human epidermal equivalent of BNIP3 knockdown keratinocytes, which suggests that BNIP3 is important for maintenance of skin epidermis. Interestingly, although UVB irradiation stimulated BNIP3 expression and cleavage of caspase3, suppression of UVB-induced BNIP3 expression led to further increase in cleaved caspase3 levels. This suggests that BNIP3 has a protective effect against UVB-induced apoptosis in keratinocytes. Overall, our data provide valuable insights into the role of BNIP3 in the differentiation and maintenance of epidermal keratinocytes.
  • Hypoxia increases gefitinib-resistant lung cancer stem cells through the activation of insulin-like growth factor 1 receptor., Akiko Murakami, Fumiyuki Takahashi, Fariz Nurwidya, Isao Kobayashi, Kunihiko Minakata, Muneaki Hashimoto, Takeshi Nara, Motoyasu Kato, Ken Tajima, Naoko Shimada, Shin-ichiro Iwakami, Mariko Moriyama, Hiroyuki Moriyama, Fumiaki Koizumi, Kazuhisa Takahashi, PloS one, PloS one, 9(1), e86459, 2014 , Refereed
    Summary:Accumulating evidence indicates that a small population of cancer stem cells (CSCs) is involved in intrinsic resistance to cancer treatment. The hypoxic microenvironment is an important stem cell niche that promotes the persistence of CSCs in tumors. Our aim here was to elucidate the role of hypoxia and CSCs in the resistance to gefitinib in non-small cell lung cancer (NSCLC) with activating epidermal growth factor receptor (EGFR) mutation. NSCLC cell lines, PC9 and HCC827, which express the EGFR exon 19 deletion mutations, were exposed to high concentration of gefitinib under normoxic or hypoxic conditions. Seven days after gefitinib exposure, a small fraction of viable cells were detected, and these were referred to as "gefitinib-resistant persisters" (GRPs). CD133, Oct4, Sox2, Nanog, CXCR4, and ALDH1A1-all genes involved in stemness-were highly expressed in GRPs in PC9 and HCC827 cells, and PC9 GRPs exhibited a high potential for tumorigenicity in vivo. The expression of insulin-like growth factor 1 (IGF1) was also upregulated and IGF1 receptor (IGF1R) was activated on GRPs. Importantly, hypoxic exposure significantly increased sphere formation, reflecting the self-renewal capability, and the population of CD133- and Oct4-positive GRPs. Additionally, hypoxia upregulated IGF1 expression through hypoxia-inducible factor 1α (HIF1α), and markedly promoted the activation of IGF1R on GRPs. Knockdown of IGF1 expression significantly reduced phosphorylated IGF1R-expressing GRPs under hypoxic conditions. Finally, inhibition of HIF1α or IGF1R by specific inhibitors significantly decreased the population of CD133- and Oct4-positive GRPs, which were increased by hypoxia in PC9 and HCC827 cells. Collectively, these findings suggest that hypoxia increased the population of lung CSCs resistant to gefitinib in EGFR mutation-positive NSCLC by activating IGF1R. Targeting the IGF1R pathway may be a promising strategy for overcoming gefitinib resistance in EGFR mutation-positive NSCLC induced by lung CSCs and microenvironment factors such as tumor hypoxia.
  • Tightly regulated and homogeneous transgene expression in human adipose-derived mesenchymal stem cells by lentivirus with tet-off system., Hiroyuki Moriyama, Mariko Moriyama, Kei Sawaragi, Hanayuki Okura, Akihiro Ichinose, Akifumi Matsuyama, Takao Hayakawa, PloS one, PloS one, 8(6), e66274, 2013 , Refereed
    Summary:Genetic modification of human adipose tissue-derived multilineage progenitor cells (hADMPCs) is highly valuable for their exploitation in therapeutic applications. Here, we have developed a novel single tet-off lentiviral vector platform. This vector combines (1) a modified tetracycline (tet)-response element composite promoter, (2) a multi-cistronic strategy to express an improved version of the tet-controlled transactivator and the blasticidin resistance gene under the control of a ubiquitous promoter, and (3) acceptor sites for easy recombination cloning of the gene of interest. In the present study, we used the cytomegalovirus (CMV) or the elongation factor 1 α (EF-1α) promoter as the ubiquitous promoter, and EGFP was introduced as the gene of interest. hADMPCs transduced with a lentiviral vector carrying either the CMV promoter or the EF-1α promoter were effectively selected by blasticidin without affecting their stem cell properties, and EGFP expression was strictly regulated by doxycycline (Dox) treatment in these cells. However, the single tet-off lentiviral vector carrying the EF-1α promoter provided more homogenous expression of EGFP in hADMPCs. Intriguingly, differentiated cells from these Dox-responsive cell lines constitutively expressed EGFP only in the absence of Dox. This single tet-off lentiviral vector thus provides an important tool for applied research on hADMPCs.
  • Occlusive dressing therapy using dimethyl sulfoxide in a patient presenting with primary localized amyloidosis of the urinary bladder: A case report, Tateki Yoshino, Shinya Ohara, Hiroyuki Moriyama, Journal of Medical Case Reports, Journal of Medical Case Reports, 7, 2013 , Refereed
    Summary:Introduction. Amyloidosis is characterized by extracellular deposition of abnormal insoluble fibrils, which cause structural and functional disorders. Amyloidosis is classified into primary and secondary disease. We report a case of localized amyloidosis of the urinary bladder. In the English literature, this is the first case effectively treated with occlusive dressing therapy using dimethyl sulfoxide. Case presentation. A 58-year-old Japanese woman was introduced to our department with asymptomatic gross hematuria. Cystoscopy revealed a gently raised nodule at the right lateral wall. Histopathological findings of this lesion revealed extensive amorphous eosinophilic deposits that stained positive with Congo red and Dylon. The patient was diagnosed with primary localized amyloidosis of the urinary bladder. To treat residual amyloidosis of the bladder, we performed occlusive dressing therapy using dimethyl sulfoxide. After treatment, cystoscopy and magnetic resonance imaging showed no relapse of the mass-like lesion of the bladder wall. Conclusions: Occlusive dressing therapy using dimethyl sulfoxide is efficacious and tolerable for amyloidosis of the urinary bladder. The maneuver of occlusive dressing therapy was simpler and easier than that of intravesical instillation, and occlusive dressing therapy was advantageous in that the patient could perform the therapy herself every day. However, invasive surgical management including cystectomy should be considered if conservative management is inefficacious. © 2013 Yoshino et al. licensee BioMed Central Ltd.
  • A Case of IgG4-Related Retroperitoneal Fibrosis Mimicking Renal Pelvic Cancer, Tateki Yoshino, Hiroyuki Moriyama, Masayuki Fukushima, Noriaki Sanda, UROLOGIA INTERNATIONALIS, UROLOGIA INTERNATIONALIS, 90(3), 365 - 368, 2013 , Refereed
    Summary:IgG4-related sclerosing disease is a novel clinicopathological entity characterized by fibrosis, extensive infiltration of IgG4-positive plasma cells, and serum IgG4 elevation. This disorder includes a variety of diseases, such as autoimmune pancreatitis, retroperitoneal fibrosis, sialadenitis, thyroiditis, inflammatory abdominal aneurysm, tubulointerstitial nephritis, and inflammatory pseudotumor [World J Gastroenterol 2008;14:3948-3955]. A 71-year-old man visited our hospital with the complaint of left flank pain and gross hematuria. Computed tomography (CT) revealed left hydronephrosis and a thick retroperitoneal soft tissue mass around the ureteropelvic junction, suspicious of renal pelvic cancer. Urine cytology using a urine sample from the left renal pelvis was negative. On laboratory examination, serum levels of IgG and IgG4 were found to be elevated. The patient refused tumor biopsy. Therefore, he was treated with corticosteroid therapy on the basis of a clinical diagnosis with IgG4-related retroperitoneal fibrosis. Regression of the retroperitoneal mass as well as improvement of left hydronephrosis and decrease in serum IgG4 levels were accomplished. These effects strongly suggested that the present case was an IgG4-related retroperitoneal fibrosis. However, in this instance, since we could not completely rule out malignancies by biopsy, careful follow-up was necessary with these points in mind. Copyright (C) 2012 S. Karger AG, Basel
  • Hypoxia induces gefitinib resistance in non-small-cell lung cancer with both mutant and wild-type epidermal growth factor receptors, Kunihiko Minakata, Fumiyuki Takahashi, Takeshi Nara, Muneaki Hashimoto, Ken Tajima, Akiko Murakami, Fariz Nurwidya, Suzu Yae, Fumiaki Koizumi, Hiroyuki Moriyama, Kuniaki Seyama, Kazuto Nishio, Kazuhisa Takahashi, CANCER SCIENCE, CANCER SCIENCE, 103(11), 1946 - 1954, Nov. 2012 , Refereed
    Summary:Somatic mutations in the epidermal growth factor receptor (EGFR) gene, such as exon 19 deletion mutations, are important factors in determining therapeutic responses to gefitinib in non-small-cell lung cancer (NSCLC). However, some patients have activating mutations in EGFR and show poor responses to gefitinib. In this study, we examined three NSCLC cell lines, HCC827, PC9, and HCC2935, that expressed an EGFR exon 19 deletion mutation. All cells expressed mutant EGFR, but the PC9 and HCC2935 cells also expressed wild-type EGFR. The HCC827 cells were highly sensitive to gefitinib under both normoxia and hypoxia. However, the PC9 and HCC2935 cells were more resistant to gefitinib under hypoxic conditions compared to normoxia. Phosphorylation of EGFR and ERK was suppressed with gefitinib treatment to a lesser extent under hypoxia. The expression of transforming growth factor-alpha (TGF alpha) was dramatically upregulated under hypoxia, and the knockdown of TGF alpha or hypoxia-inducible factor-1 alpha (HIF1 alpha) reversed the resistance to gefitinib in hypoxic PC9 and HCC2935 cells. Finally, introduction of the wild-type EGFR gene into the HCC827 cells caused resistance to gefitinib under hypoxia. This phenomenon was also reversed by the knockdown of TGF alpha or HIF1 alpha. Our results indicate that hypoxia causes gefitinib resistance in EGFR-mutant NSCLC through the activation of wild-type EGFR mediated by the upregulation of TGF alpha. The presence of wild-type and mutant EGFR along with tumor hypoxia are important factors that should be considered when treating NSCLC patients with gefitinib. (Cancer Sci 2012; 103: 1946-1954)
  • Human adipose tissue-derived multilineage progenitor cells exposed to oxidative stress induce neurite outgrowth in PC12 cells through p38 MAPK signaling., Mariko Moriyama, Hiroyuki Moriyama, Ayaka Ueda, Yusuke Nishibata, Hanayuki Okura, Akihiro Ichinose, Akifumi Matsuyama, Takao Hayakawa, BMC cell biology, BMC cell biology, 13, 21 - 21, Aug. 07 2012 , Refereed
    Summary:BACKGROUND: Adipose tissues contain populations of pluripotent mesenchymal stem cells that also secrete various cytokines and growth factors to support repair of damaged tissues. In this study, we examined the role of oxidative stress on human adipose-derived multilineage progenitor cells (hADMPCs) in neurite outgrowth in cells of the rat pheochromocytoma cell line (PC12). RESULTS: We found that glutathione depletion in hADMPCs, caused by treatment with buthionine sulfoximine (BSO), resulted in the promotion of neurite outgrowth in PC12 cells through upregulation of bone morphogenetic protein 2 (BMP2) and fibroblast growth factor 2 (FGF2) transcription in, and secretion from, hADMPCs. Addition of N-acetylcysteine, a precursor of the intracellular antioxidant glutathione, suppressed the BSO-mediated upregulation of BMP2 and FGF2. Moreover, BSO treatment caused phosphorylation of p38 MAPK in hADMPCs. Inhibition of p38 MAPK was sufficient to suppress BMP2 and FGF2 expression, while this expression was significantly upregulated by overexpression of a constitutively active form of MKK6, which is an upstream molecule from p38 MAPK. CONCLUSIONS: Our results clearly suggest that glutathione depletion, followed by accumulation of reactive oxygen species, stimulates the activation of p38 MAPK and subsequent expression of BMP2 and FGF2 in hADMPCs. Thus, transplantation of hADMPCs into neurodegenerative lesions such as stroke and Parkinson's disease, in which the transplanted hADMPCs are exposed to oxidative stress, can be the basis for simple and safe therapies.
  • In Situ Stem Cell Therapy Using Human Adipose Tissue-Derived Multi-lineage Progenitor Cells Combined with HMG-CoA Reductase Inhibitor Synergistically Reduce Serum Cholesterol Level in Hyperlipidemic Watanabe Rabbits, Hanayuki Okura, Ayami Saga, Mayumi Soeda, Jyunko Tani, Mariko Moriyama, Hiroyuki Moriyama, Shizuya Yamashita, Akihiro Ichinose, Shinya Tahara, Takao Hayakawa, Akifumi Matsuyama, CIRCULATION, CIRCULATION, 124(21), Nov. 2011 , Refereed
  • Transplantation of Adipose Tissue-Derived Multi-Lineage Progenitor Cells Reduces Serum Cholesterol in Hyperlipidemic Watanabe Rabbits, Hanayuki Okura, Ayami Saga, Mayumi Soeda, Jyunko Tani, Mariko Moriyama, Hiroyuki Moriyama, Sihizuya Yamashita, Akihiro Ichinose, Shinya Tahara, Takao Hayakawa, Akifumi Matsuyama, CIRCULATION, CIRCULATION, 124(21), Nov. 2011 , Refereed
  • HMG-CoA reductase inhibitor augments the serum total cholesterol-lowering effect of human adipose tissue-derived multilineage progenitor cells in hyperlipidemic homozygous Watanabe rabbits., Ayami Saga, Hanayuki Okura, Mayumi Soeda, Junko Tani, Yuichi Fumimoto, Hiroshi Komoda, Mariko Moriyama, Hiroyuki Moriyama, Shizuya Yamashita, Akihiro Ichinose, Takashi Daimon, Takao Hayakawa, Akifumi Matsuyama, Biochemical and biophysical research communications, Biochemical and biophysical research communications, 412(1), 50 - 4, Aug. 19 2011 , Refereed
    Summary:Familial hypercholesterolemia (FH) is an autosomal codominant disease characterized by high concentrations of proatherogenic lipoproteins secondary to deficiency in low-density lipoprotein (LDL) receptor. We reported recently the use of in situ stem cell therapy of human adipose tissue-derived multilineage progenitor cells (hADMPCs) in lowering serum total cholesterol in the homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model of homozygous FH. Here we demonstrate that pravastatin, an HMG-CoA reductase inhibitor, augmented the cholesterol-lowering effect of transplanted hADMPCs and enhanced LDL clearance in homozygous WHHL rabbit. The results suggest the potential beneficial effects of in situ stem cell therapy in concert with appropriately selected pharmaceutical agents, in regenerative medicine.
  • Transplantation of human adipose tissue-derived multilineage progenitor cells reduces serum cholesterol in hyperlipidemic Watanabe rabbits., Hanayuki Okura, Ayami Saga, Yuichi Fumimoto, Mayumi Soeda, Mariko Moriyama, Hiroyuki Moriyama, Koji Nagai, Chun-Man Lee, Shizuya Yamashita, Akihiro Ichinose, Takao Hayakawa, Akifumi Matsuyama, Tissue engineering. Part C, Methods, Tissue engineering. Part C, Methods, 17(2), 145 - 54, Feb. 2011 , Refereed
    Summary:Familial hypercholesterolemia (FH) is an autosomal codominant disease characterized by high concentrations of proatherogenic lipoproteins and premature atherosclerosis secondary to low-density lipoprotein (LDL) receptor deficiency. We examined a novel cell therapy strategy for the treatment of FH in the Watanabe heritable hyperlipidemic (WHHL) rabbit, an animal model for homozygous FH. We delivered human adipose tissue-derived multilineage progenitor cells (hADMPCs) via portal vein and followed by immunosuppressive regimen to avoid xenogenic rejection. Transplantation of hADMPCs resulted in significant reductions in total cholesterol, and the reductions were observed within 4 weeks and maintained for 12 weeks. (125)I-LDL turnover study showed that the rate of LDL clearance was significantly higher in the WHHL rabbits with transplanted hADMPCs than those without transplanted. After transplantation hADMPCs were localized in the portal triad, subsequently integrated into the hepatic parenchyma. The integrated cells expressed human albumin, human alpha-1-antitrypsin, human Factor IX, human LDL receptors, and human bile salt export pump, indicating that the transplanted hADMPCs resided, survived, and showed hepatocytic differentiation in vivo and lowered serum cholesterol in the WHHL rabbits. These results suggested that hADMPC transplantation could correct the metabolic defects and be a novel therapy for inherited liver diseases.
  • Multiple roles of notch signaling in the regulation of epidermal development, Mariko Moriyama, Andre-Dante Durham, Hiroyuki Moriyama, Kiyotaka Hasegawa, Shin-Ichi Nishikawa, Freddy Radtke, Masatake Osawa, DEVELOPMENTAL CELL, DEVELOPMENTAL CELL, 14(4), 594 - 604, Apr. 2008 , Refereed
    Summary:Recent studies have shown that Notch signaling plays an important role in epidermal development, but the underlying molecular mechanisms remain unclear. Here, by integrating loss- and gain -of-function studies of Notch receptors and Hes1, we describe molecular information about the role of Notch signaling in epidermal development. We show that Notch signaling determines spinous cell fate and induces terminal differentiation by a mechanism independent of Hes1, but Hes1 is required for maintenance of the immature state of spinous cells. Notch signaling induces Ascl2 expression to promote terminal differentiation, while simultaneously repressing Ascl2 through Hes1 to inhibit premature terminal differentiation. Despite the critical role of Hes1 in epidermal development, Hes1 null epidermis transplanted to adult mice showed no obvious defects, suggesting that this role of Hes1 may be restricted to developmental stages. Overall, we conclude that Notch signaling orchestrates the balance between differentiation and immature programs in suprabasal cells during epidermal development.
  • Rapid up-regulation of c-FLIP expression by BCR signaling through the PI3K/Akt pathway inhibits simultaneously induced Fas-mediated apoptosis in murine B lymphocytes., Hiroyuki Moriyama, Shin Yonehara, Immunology letters, Immunology letters, 109(1), 36 - 46, Mar. 15 2007 , Refereed
    Summary:Cross-linking of BCR rapidly induces protection of B cells from Fas-mediated apoptosis, which has been assumed one of the important survival mechanisms of B cells during antigen stimulation. In the mouse B cell line A20, which is sensitive to Fas-mediated apoptosis, stimulation of BCR inhibited apoptosis induced via Fas upstream of caspase-8 activation with an associated rapid increase in the expression of both short and long forms of cellular caspase-8/FLICE-inhibitory protein (c-FLIP). The c-FLIP competitively inhibited the recruitment of caspase-8 to the death-inducing signaling complex (DISC), which took as long as 3h to form after the stimulation of Fas in A20 cells. Knockdown of c-FLIP by a short hairpin RNA-expressing method rendered BCR-stimulated A20 cells sensitive to Fas-mediated apoptosis. The BCR-induced rapid expression of c-FLIP was not affected by inactivation of NF-kappaB, but was inhibited by either treatment with a PI3K inhibitor, LY294002, or expression of a dominant negative PI3K p85 subunit, both of which suppressed phosphorylation of Akt and sensitized BCR-stimulated A20 cells to Fas-mediated apoptosis. Overexpression of constitutively active Akt was shown not only to up-regulate c-FLIP expression but also to render A20 cells resistant to Fas-mediated apoptosis. Moreover, treatment with LY294002 also suppressed BCR-induced up-regulation of c-FLIP expression in spleen B cells. Taken together, BCR-stimulation was shown to rapidly trigger a survival signal against simultaneously or ongoingly stimulated Fas-mediated apoptosis by promoting a PI3K/Akt signaling pathway-mediated up-regulation of c-FLIP expression.
  • Genetic subtypes of HIV type 1 in Republic of Congo., B Bikandou, J Takehisa, I Mboudjeka, E Ido, T Kuwata, Y Miyazaki, H Moriyama, Y Harada, Y Taniguchi, H Ichimura, M Ikeda, P J Ndolo, M Y Nzoukoudi, R M'Vouenze, M M'Pandi, H J Parra, P M'Pelé, M Hayami, AIDS research and human retroviruses, AIDS research and human retroviruses, 16(7), 613 - 9, May 01 2000 , Refereed
    Summary:To assess the molecular epidemiology of HIV-1 in Republic of Congo (Congo), we investigated 29 HIV-1s obtained from 82 Congolese AIDS and ARC patients in 1996 and 1997. Part of the env region including the V3 loop was phylogenetically analyzed. The genotypes observed were varied: of 29 specimens, 12 (41 %) were subtype A, 1 (3%) was subtype D, 6 (21%) were subtype G, 6 (21%) were subtype H, 2 (7%) were subtype J, and 2 (7%) could not be classified as any known subtypes (U, unclassified). The heterogeneous profile of HIV-1 infection was different from the profiles of neighboring Central African countries. These data show that subtypes G and H as well as subtype A were circulating with high prevalence. The fact that new genetic subtypes (J and U) are circulating indicates a need for a greater surveillance for these subtypes both in Congo as well as in other parts of the world.
  • Various types of HIV mixed infections in Cameroon., J Takehisa, L Zekeng, E Ido, I Mboudjeka, H Moriyama, T Miura, M Yamashita, L G Gürtler, M Hayami, L Kaptué, Virology, Virology, 245(1), 1 - 10, May 25 1998 , Refereed
    Summary:In order to assess the incidence of HIV mixed infection as well as to clarify the molecular epidemiology of HIV in central Africa, we investigated 43 HIVs obtained from 211 Cameroonian AC, ARC, and AIDS patients in 1994 and 1995. Part of the pol region and part of the env region were phylogenetically analyzed. The genotypes observed were varied: of 43 specimens, 28 (65%) were subtype A, 1 (2%) was subtype B, 2 (5%) were subtype D, 3 (7%) were subtype F, and 2 (5%) were group O. Of the remaining 7 specimens, 3 were mixed infections with HIV-1 subtypes A and C, HIV-1 subtypes C and F, and HIV-2 subtype A and HIV-1 subtype A; 1 was a mixed infection with HIV-1 subtypes A and D and the highly divergent group O (triple infection); another 3 appeared to consist of mosaic genomes (A/G, A/E, and B/A recombinant). These data show that various types of mixed infection, such as between different subtypes of HIV-1 group M, between HIV-1 and HIV-2, and even between HIV-1 groups O and M, were confirmed at a rather high frequency (approximately 10%). The mixed infection is particularly significant where there is a greater variety of HIV-1 subtypes circulating, since it results in new genetic diversity generated by intersubtype recombination.
  • Infectivity and immunogenicity of SIVmac/HIV-1 chimeric viruses (SHIVs) with deletions in two or three genes (vpr, nef and vpx)., T Igarashi, T Kuwata, H Yamamoto, H Moriyama, M Ui, Y Miyazaki, M Hayami, Microbiology and immunology, Microbiology and immunology, 42(1), 71 - 4, 1998 , Refereed
    Summary:Two SHIVs with two or three genes deleted (SHIV-drn and SHIV-dxrn) were constructed. The inoculation of monkeys with SHIV-drn resulted in short-term viremia, but inoculation with SHIV-dxrn did not. At 68 weeks post-inoculation, the monkeys were reinoculated with a 100-fold higher dose of each SHIV, but none showed viremia. Killer cell activities against HIV-1 Env were detected in the SHIV-drn- and SHIV-dxrn-inoculated monkeys. Cross-reactive killer activity against HIV-1 Gag and SIVmac Gag was observed in one monkey. Antibodies were not detected in the SHIV-dxrn-inoculated monkeys, but the SHIV-drn-inoculated monkeys showed an anamnestic antibody reaction. These data indicate that SHIV-drn is infectious to and immuno-inducible in macaques but SHIV-dxrn is not.

Misc

  • Potential of autophagy in cosmetics application, 森山麻里子, 森山博由, Fragrance Journal, 47, 8, 12, 19,   2019 08 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201902221192312391
  • Potential of autophagy in cosmetics application, 森山 麻里子, 森山 博由, Fragrance journal : Research & development for cosmetics, toiletries & allied industries = フレグランスジャーナル : 香粧品科学研究開発専門誌, 47, 8, 12, 19,   2019 08 , http://ci.nii.ac.jp/naid/40021995585
  • 皮膚組織における血管構築の規則性と加齢に伴う破綻, 高島さつき, 高島さつき, 鈴木真理子, 森山麻里子, 市橋正光, 岡本正志, 依馬正次, 森山博由, 水谷健一, 日本薬学会年会要旨集(CD-ROM), 139th, 3, ROMBUNNO.23P‐am05S, 87,   2019 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201902254711622135
  • iPS細胞・幹細胞を用いた皮膚メカニズム解明と化粧品評価技術 脂肪由来幹細胞の化粧品評価への活用技術の動向, 森山博由, 森山麻里子, 早川堯夫, 隔月刊Cosmetic Stage, 13, 3, 31‐39,   2019 02 25 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201902284864248827
  • アロエベラ液汁による紫外線ダメージ軽減効果, 森山麻里子, 赤木淳二, 北郡秀晃, 森山博由, Bio Industry, 35, 9, 27‐35,   2018 09 12 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201802260652018342
  • 混合植物エキスによる加齢に伴う表皮菲薄化の抑制アプローチ, 岩野英生, 森山麻里子, 陳玉倩, 呂梨萍, 沈柏村, 森山博由, 澤木茂豊, 日本皮膚科学会雑誌, 128, 5, 1174, 1174,   2018 05 , http://jglobal.jst.go.jp/public/201802215036635462
  • BNIP3は紫外線から皮膚を保護する際に重要な役割を果たす, 森田 遼, 森山 麻里子, 森田 貴士, 丸谷 祐樹, 後藤 ありさ, 松本 諭以子, 夏賀 健, 早川 堯夫, 森山 博由, 日本薬学会年会要旨集, 138年会, 3, 133, 133,   2018 03
  • 薬学部実務実習生を対象にした処方解析プログラムの効果の検証について, 齋藤 玲奈, 阿登 大次郎, 清水 忠, 森山 博由, 小竹 武, 井上 知美, 小森 浩二, 三田村 しのぶ, 日高 眞理, 廣瀬 隆, 吉田 彰彦, 小牟田 豊, 東海 秀吉, 交通医学, 72, 1-2, 17, 17,   2018 03
  • 薬学部実務実習生を対象にした処方解析プログラムの効果の検証について, 齋藤 玲奈, 阿登 大次郎, 清水 忠, 森山 博由, 小竹 武, 井上 知美, 小森 浩二, 三田村 しのぶ, 日高 眞理, 廣瀬 隆, 吉田 彰彦, 小牟田 豊, 東海 秀吉, 交通医学, 72, 1-2, 17, 17,   2018 03
  • 皮膚組織における幹細胞の維持に血管が果たす役割, 高島さつき, 鈴木真理子, 森山麻里子, 森山博由, 岡本正志, 市橋正光, 水谷健一, 日本薬学会年会要旨集(CD-ROM), 138年会, 3, 172, 172,   2018 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201802219222111582
  • BNIP3は紫外線から皮膚を保護する際に重要な役割を果たす, 森田遼, 森山麻里子, 森田貴士, 丸谷祐樹, 後藤ありさ, 松本諭以子, 夏賀健, 早川堯夫, 森山博由, 日本薬学会年会要旨集(CD-ROM), 138年会, 3, 133, 133,   2018 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201802241011776257
  • 低酸素状態に維持されたヒト脂肪由来幹細胞における新たな解糖系制御機構, 森山博由, 森山麻里子, 早川堯夫, 日本再生医療学会総会(Web), 17th, ROMBUNNO.O‐29‐1 (WEB ONLY),   2018 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201802231568232104
  • 皮膚組織における規則的な血管構築は,加齢と共に変化する, 高島さつき, 高島さつき, 上野顕平, 上野顕平, 鈴木真理子, 森山麻里子, 森山博由, 岡本正志, 市橋正光, 水谷健一, 日本分子生物学会年会プログラム・要旨集(Web), 41st, ROMBUNNO.2P‐0465 (WEB ONLY),   2018 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201802248159473772
  • オートファジー制御因子BNIP3は表皮恒常性の維持に寄与する, 森田貴士, 森山麻里子, 後藤ありさ, 森田遼, 丸谷祐樹, 松本諭以子, 早川堯夫, 森山博由, 日本再生医療学会総会(Web), 17th, ROMBUNNO.O‐14‐3 (WEB ONLY),   2018 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201802284203514639
  • 低酸素条件下での脂肪組織由来間葉系幹細胞におけるNotchシグナルの役割, 井上 翔, 森山 麻里子, 木村 徳仁, 藤村 朱美香, 和多田 巧, 小澤 俊之, 早川 堯夫, 森山 博由, 生命科学系学会合同年次大会, 2017年度, [4LT19, 0447)],   2017 12
  • FoxO3aはオートファジーを介して創傷治癒に影響を及ぼす, 森田 貴士, 森山 麻里子, 後藤 ありさ, 森田 遼, 丸谷 祐樹, 松本 諭以子, 早川 堯夫, 森山 博由, 生命科学系学会合同年次大会, 2017年度, [4P1T19, 0353)],   2017 12
  • Bnip3が誘導するオートファジーは紫外線ストレスから表皮を保護する, 丸谷祐樹, 森山麻里子, 森田貴士, 後藤ありさ, 森田遼, 松本諭以子, 夏賀健, 早川堯夫, 森山博由, 日本生化学会大会(Web), 2017年度, [1P, 0561],   2017 12 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201702238990415158
  • iPS細胞・再生医療 ヒト脂肪を由来とした再生医療用細胞原材料の開発, 森山博由, 森山麻里子, 早川堯夫, 月刊PHARM STAGE, 17, 6, 2‐6, 6,   2017 09 15 , http://jglobal.jst.go.jp/public/201802244368092372
  • アロエベラ液汁による皮膚への紫外線ダメージ低減効果, 丸谷 祐樹, 森山 麻里子, 森田 貴士, 後藤 ありさ, 田島 史郎, 赤木 淳二, 國友 栄治, 上田 太郎, 松岡 信也, 冨永 剛, 森山 博由, 日本生薬学会年会講演要旨集, 64回, 254, 254,   2017 08
  • アロエベラ液汁による皮膚浸透性の改善作用, 田島 史郎, 赤木 淳二, 中田 孝広, 森山 麻里子, 後藤 ありさ, 森田 貴士, 中島 佑香, 森田 遼, 福田 敬子, 冨永 剛, 國友 栄治, 上田 太郎, 松岡 信也, 早川 堯夫, 森山 博由, Aesthetic Dermatology, 27, 2, 219, 219,   2017 07
  • FoxO3aの皮膚における機能, 森田貴士, 森山麻里子, 後藤ありさ, 森田遼, 早川堯夫, 森山博由, 日本薬学会年会要旨集(CD-ROM), 137年会, 3, 122, 122,   2017 03 , http://jglobal.jst.go.jp/public/201702281644998305
  • bcl2ファミリー分子BNIP3はオートファジーを介した表皮における形態維持を担う, 丸谷 祐樹, 森山 麻里子, 森田 貴士, 中島 佑香, 後藤 ありさ, 森田 遼, 夏賀 健, 早川 堯夫, 森山 博由, 日本薬学会年会要旨集, 137年会, 3, 152, 152,   2017 03
  • アロエベラ液汁による皮膚浸透促進効果, 赤木淳二, 森山麻里子, 後藤ありさ, 森田貴士, 中島佑香, 森田遼, 福田敬子, 國友栄治, 上田太郎, 松岡信也, 早川堯夫, 森山博由, 日本薬学会年会要旨集(CD-ROM), 137年会, 3, 160, 160,   2017 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201702240959409989
  • 低酸素状態下でのヒト脂肪由来間葉系幹細胞におけるNotchシグナルの役割, 井上翔, 森山麻里子, 野澤一輝, 木村徳仁, 藤村朱美香, 小澤俊幸, 早川堯夫, 森山博由, 日本薬学会年会要旨集(CD-ROM), 137年会, 3, 162, 162,   2017 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201702250807952908
  • 低酸素状態下のヒト間葉系幹細胞維持機構におけるNotchシグナルの役割, 森山博由, 森山麻里子, 大倉華雪, 松山晃文, 早川堯夫, 再生医療, 16, 272,   2017 02 01 , http://jglobal.jst.go.jp/public/201702215180330001
  • オートファジー制御を担うBNIP3は健全な皮膚形成に必要である, 森山麻里子, 森田貴士, 久保嘉一, 後藤ありさ, 早川堯夫, 森山博由, 再生医療, 16, 349,   2017 02 01 , http://jglobal.jst.go.jp/public/201702256882173390
  • アロエベラ液汁の美肌効果, 森山麻里子, 森山麻里子, 赤木淳二, 森山博由, Bio Industry, 33, 4, 54‐59,   2016 04 12 , http://jglobal.jst.go.jp/public/201602203330077340
  • Beauty is Skin Deep : the Fascinating Effects of Aloe Vera Gel on the Epidermis, 森山 麻里子, 赤木 淳二, 森山 博由, Bio industry = バイオインダストリー, 33, 4, 54, 59,   2016 04 , http://ci.nii.ac.jp/naid/40021176048
  • bc12ファミリー分子BNIP3はオートファジーを介して表皮の分化および形態維持を行う, 久保 嘉一, 森山 麻里子, 中島 佑香, 後藤 ありさ, 夏賀 健, 早川 堯夫, 森山 博由, 日本薬学会年会要旨集, 136年会, 3, 146, 146,   2016 03
  • アロエ属植物の皮膚修復作用メカニズムに関する研究, 後藤ありさ, 森山麻里子, 久保嘉一, 中島佑香, 赤木淳二, 赤木淳二, 吉田郁代, 中村行雄, 早川堯夫, 森山博由, 日本薬学会年会要旨集(CD-ROM), 136年会, 3, 183, 183,   2016 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201602211652168440
  • bcl2ファミリー分子BNIP3はオートファジーを介して表皮の分化および形態維持を行う, 久保嘉一, 森山麻里子, 中島佑香, 後藤ありさ, 夏賀健, 早川堯夫, 森山博由, 日本薬学会年会要旨集(CD-ROM), 136th, ROMBUNNO.29AB‐AM260S,   2016 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201602254099594843
  • bcl2ファミリー分子BNIP3はオートファジーを介して表皮の分化および形態維持を行う, 森田貴士, 森山麻里子, 中島佑香, 後藤ありさ, 森田遼, 夏賀健, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 39th, ROMBUNNO.2P‐0560 (WEB ONLY),   2016 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201702227518365330
  • 幹細胞を用いた最新のエイジングケア研究と化粧品開発 間葉系幹細胞の化粧品評価への活用展望, 森山博由, 森山麻里子, 早川堯夫, 隔月刊Cosmetic Stage, 9, 8, 24‐28,   2015 12 25 , http://jglobal.jst.go.jp/public/201602218436776422
  • 低酸素状態下のヒト間葉系幹細胞維持機構におけるNotchシグナルの役割, 百合祐樹, 森山麻里子, 石原慎, 大倉華雪, 松山晃文, 早川堯夫, 森山博由, 日本生化学会大会(Web), 88回・38回, [4T11L, 10(3P0984)],   2015 12 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201602204553914720
  • オートファジー制御関連分子BNIP3は紫外線による過度の皮膚傷害から表皮を防御する, 久保嘉一, 森山麻里子, 中島佑香, 後藤ありさ, 早川堯夫, 森山博由, 日本生化学会大会(Web), 88回・38回, [4T6L, 06(3P0226)],   2015 12 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201602211179243596
  • Roles of Autophagy-Related Gene in Differentiation and Maintenance of Epidermis, 森山麻里子, 森山麻里子, 森山博由, 早川堯夫, 日本香粧品学会誌, 39, 3, 192, 195,   2015 09 , 10.11469/koshohin.39.192, http://jglobal.jst.go.jp/public/201502210063799739
    Summary:<p>The skin epidermis is a stratified epithelium. Recent studies have clarified a numerous number of molecules involved in epidermal development, although it remains elusive how these molecules are coordinated to undergo proper stratification of the epidermis. Autophagy, a lysosomal degradation pathway, is involved in differentiation of erythrocytes, lymphocytes, and adipocytes. Keratinocyte differentiation is also going along with activation of lysosomal enzymes and organelle clearance, expecting the contribution of autophagy in this process. Previously, we show multiple roles of Notch signaling in the regulation of transit amplifying cells in epidermal layers. Notch signaling induces differentiation of suprabasal cells <i>via</i> Hes1 independent manner, whereas Hes1 is required for maintenance of the immature status of suprabasal cells by preventing premature differentiation. In this study, we found that Hes1 directly suppressed the expression of Bnip3, whose expression is sufficient to induce terminal differentiation of keratinocytes by induction of autophagy. We found that HES1 could directly bind to <i>BNIP3</i> promoter to suppress the expression. BNIP3 was expressed in the granular layers, just above the layers where Hes1 expression was observed. Consistent with the BNIP3 expression, autophagosome formation was observed in the granular layer of the epidermis. Forced expression of BNIP3 in human primary epidermal keratinocytes (HPEK) resulted in induction of autophagy and mitophagy, followed by keratinocyte differentiation. Intriguingly, addition of an inhibitor of autophagy significantly suppressed the BNIP3-stimulated differentiation of keratinocytes. These data clearly indicate that BNIP3 plays a crucial role in keratinocytes differentiation by inducing autophagy. Furthermore, we also found that suppression of BNIP3 expression induced by UVB irradiation caused a further increase of the cleaved caspase3 protein level, suggesting that BNIP3 also has a protective effect against UVB-induced apoptosis in keratinocytes. Overall, our data shed light on functions of BNIP3, regulated by Notch signaling, in both differentiation and maintenance of epidermal keratinocytes.</p>
  • アロエベラによるヒト皮膚修復作用機序~初代ヒト表皮角化細胞を用いた実効評価~, 後藤ありさ, 森山麻里子, 久保嘉一, 中島佑香, 赤木淳二, 吉田郁代, 中村行雄, 森山博由, 和漢医薬学会学術大会要旨集, 32回, 95, 95,   2015 08 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201502214479243220
  • 家族性高コレステロール血症に対する新しい治療法の開発と臨床応用, 小関正博, 小関正博, 嵯峨礼美, 嵯峨礼美, 江副幸子, 小林卓哉, 朝治真澄, 松田響, 朱頴こう, 岡田健志, 西良雅己, 中谷和弘, 川瀬良太, 増田大作, 大濱透, 大濱透, 西田誠, 西田誠, 冨田興一, 細川亙, 大須賀慶悟, 富山憲幸, 川本弘一, 伊藤壽記, 柳光司, 市育代, 森山博由, 早川堯夫, 荒井秀典, 斯波真理子, 坂田泰史, 山下静也, 山下静也, 日本動脈硬化学会総会・学術集会プログラム・抄録集(Web), 47th, 113 (WEB ONLY),   2015 06 25 , http://jglobal.jst.go.jp/public/201502205414288899
  • 我が国の原発性高脂血症の現状と未来 家族性高コレステロール血症に対する新しい治療法の開発と臨床応用, 小関 正博, 嵯峨 礼美, 江副 幸子, 小林 卓哉, 朝治 真澄, 松田 響, 朱 頴こう, 岡田 健志, 西良 雅己, 中谷 和弘, 川瀬 良太, 増田 大作, 大濱 透, 西田 誠, 冨田 興一, 細川 亙, 大須賀 慶悟, 富山 憲幸, 川本 弘一, 伊藤 壽記, 柳 光司, 市 育代, 森山 博由, 早川 堯夫, 荒井 秀典, 斯波 真理子, 坂田 泰史, 山下 静也, 日本動脈硬化学会総会プログラム・抄録集, 47回, 113, 113,   2015 06
  • bcl2ファミリー分子BNIP3は,オートファジーを介して上皮の分化および形態維持を行う。, 久保嘉一, 森山麻里子, 宇田純輝, 早川堯夫, 森山博由, 日本薬学会年会要旨集(CD-ROM), 135年会, 3, 171, 171,   2015 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201502251747678032
  • 低酸素状態を経た脂肪由来間葉系幹細胞機能亢進の不可逆性~Notchシグナルと解糖系調節機構~, 森山博由, 森山麻里子, 小澤俊幸, 大倉華雪, 松山晃文, 早川堯夫, 再生医療, 14, 247,   2015 02 01 , http://jglobal.jst.go.jp/public/201502294953109835
  • オートファジー制御を担うBNIP3は健全な皮膚形成に必要である, 森山麻里子, 宇田純輝, 森山博由, 早川尭夫, 再生医療, 14, 271,   2015 02 01 , http://jglobal.jst.go.jp/public/201502259359489105
  • ヒト幹細胞の造腫瘍性における病態解明とその克服に関する研究 各種細胞調製と特性評価, 早川堯夫, 森山博由, 森山麻里子, ヒト幹細胞の造腫瘍性における病態解明とその克服に関する研究 平成26年度 総括・分担研究報告書, 51‐76,   2015 , http://jglobal.jst.go.jp/public/201602210082181173
  • LDLアフェレーシス療法施行中の重症家族性高コレステロール血症に対する,同種脂肪組織由来多系統前駆細胞(ADMPC)を用いた細胞移植療法の確立 ADMPCの安全性の検討(安全性確保に関する助言), 早川堯夫, 森山博由, LDLアフェレーシス療法施行中の重症家族性高コレステロール血症に対する、同種脂肪組織由来多系統前駆細胞(ADMPC)を用いた細胞移植療法の確立 平成26年度 委託業務成果報告書, 141‐149,   2015 , http://jglobal.jst.go.jp/public/201602211953962444
  • 脂肪由来幹細胞の特徴と脂肪細胞移植における基礎研究からの留意点, 森山博由, DDS再生医療研究会プログラム・抄録集(Web), 5th, ROMBUNNO.TOKUBETSUKOENI (WEB ONLY),   2015 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201802258736045292
  • オートファジー制御関連分子BNIP3は表皮分化ならびに表皮形態維持に重要な働きをする, 森山麻里子, 森山博由, 宇田純輝, 大沢匡毅, 松山晃文, 早川堯夫, 再生医療, 13, 335,   2014 01 27 , http://jglobal.jst.go.jp/public/201402282138231531
  • 低酸素暴露を介する脂肪由来間葉系幹細胞のドパミン産生細胞分化誘導, 森山博由, 森山麻里子, 大森重成, 大倉華雪, 松山晃文, 早川堯夫, 再生医療, 13, 240,   2014 01 27 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402214895111270
  • 再生医療早期実用化促進及び汎用性向上のための周辺基盤技術開発 細胞・組織加工製品の感染制御法の開発(及び免疫原性制御法の開発/均質性・同等性確保の方策の検討), 早川堯夫, 森山博由, 森山麻里子, 上森隆司, 橋爪克仁, 再生医療早期実用化促進及び汎用性向上のための周辺基盤技術開発 平成25年度 総括・分担研究報告書, 57, 75,   2014 , http://jglobal.jst.go.jp/public/201402249671942329
  • ヒト幹細胞の造腫瘍性における病態解明とその克服に関する研究 各種細胞調製と特性評価, 早川堯夫, 森山博由, 森山麻里子, ヒト幹細胞の造腫瘍性における病態解明とその克服に関する研究 平成25年度 総括・分担研究報告書, 31‐51,   2014 , http://jglobal.jst.go.jp/public/201602268245929292
  • ヒト脂肪組織由来多系統前駆細胞(hADMPC)を用いたドパミン産生細胞への誘導法の確立, 大森重成, 森山麻里子, 谷口祐紀, 深瀬尭哉, 松山晃文, 早川堯夫, 森山博由, 生体機能と創薬シンポジウム要旨集, 2014, 105,   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402209102184970
  • キンドラー症候群患者由来ヒト脂肪組織由来多系統前駆細胞(hADMPC)より樹立したiPS細胞の皮膚ケラチノサイトへの分化誘導法確立, 谷口祐紀, 森山麻里子, 大森重成, 早川堯夫, 森山博由, 生体機能と創薬シンポジウム要旨集, 2014, 136,   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402227825279950
  • 幹細胞資材におけるウイルス混入及び残存試験法確立を目的とした高感度・高精度な新規核酸増幅基盤技術開発, 河野真有香, 森山麻里子, 中北和樹, 早川堯夫, 森山博由, 生体機能と創薬シンポジウム要旨集, 2014, 152,   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402244694658693
  • BCL‐2ファミリー分子BNIP3が表皮分化および表皮形態維持に及ぼす影響, 山田翼, 森山麻里子, 宇田純輝, 森山博由, 早川堯夫, 生体機能と創薬シンポジウム要旨集, 2014, 119,   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402255395929704
  • 新規ヒト脂肪組織由来多系統前駆細胞(hADMPC)を用いたインスリン産生細胞の作製, 曽根千晶, 森山麻里子, 大倉華雪, 松山晃文, 早川尭夫, 森山博由, 生体機能と創薬シンポジウム要旨集, 2014, 135,   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402260926948028
  • 低酸素状態におけるNotchシグナルと解糖系の関係, 石原慎, 森山麻里子, 阪口公一, 石濱里穂, 大倉華雪, 松山晃文, 早川堯夫, 森山博由, 生体機能と創薬シンポジウム要旨集, 2014, 133,   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402278447111780
  • 新規ヒト脂肪組織由来多能性前駆細胞に存在するOCT4陽性細胞は真の多能性幹細胞たりうるのか?, 百合祐樹, 森山麻里子, 早川堯夫, 森山博由, 生体機能と創薬シンポジウム要旨集, 2014, 121,   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402287993994072
  • オートファジー制御関連分子BNIP3は表皮分化ならびに表皮形態維持に重要な働きをする, 宇田純輝, 森山麻里子, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 37th, 3W13-2(3P-0529) (WEB ONLY),   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201502202988549046
  • タイ天然薬物Shorea roxburghii樹皮由来オリゴスチルベノイドは悪性黒色腫に対して抗がん作用を示す, 石濱里穂, 道山忠史, 森山麻里子, 村岡修, 二宮清文, 早川堯夫, 森川敏夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 37th, 2P-0831 (WEB ONLY),   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201502224280143345
  • 低酸素状態下のヒト間葉系幹細胞維持機構におけるNotchシグナルの役割, 石原慎, 森山麻里子, 阪口公一, 大倉華雪, 松山晃文, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 37th, 3W13-8(3P-0535) (WEB ONLY),   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201502250670078073
  • 新規ヒト脂肪組織由来多系統前駆細胞(hADMPC)を用いたインスリン産生細胞の作製, 曽根千晶, 森山麻里子, 大倉華雪, 松山晃文, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 37th, 2P-0571 (WEB ONLY),   2014 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201502266708674183
  • 低酸素暴露下における脂肪由来間葉系幹細胞のNotchシグナル亢進と解糖系調節機構の解明, 森山博由, 森山麻里子, 一志春樹, 大倉華雪, 松山晃文, 早川堯夫, 再生医療, 12, 233,   2013 02 28 , http://jglobal.jst.go.jp/public/201302293646711713
  • Bcl‐2ファミリー分子BNIP3が表皮構築に及ぼす影響, 宇田純輝, 森山麻里子, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 36th, 2P-0574 (WEB ONLY),   2013 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402216755738489
  • 再生医療実用化に向けた幹細胞の安全性評価―複合糖質糖鎖の網羅解析の適用―, 保村佳孝, 木下充弘, 館山大揮, 菅三佳, 古江美保, 森山博由, 早川堯夫, 掛樋一晃, 日本薬学会年会要旨集, 132年会, 3, 184, 184,   2012 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201202215616721147
  • 表皮組織の形態維持と分化にはBNIP3を介したオートファジーが必須である, 宇田純輝, 森山麻里子, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 35th, 4P-0420 (WEB ONLY),   2012 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201302217051459109
  • 低酸素下におけるNotchシグナルによる解糖系調節機構の解明, 一志春樹, 森山麻里子, 椹木桂, 大倉華雪, 松山晃文, 掛樋一晃, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 35th, 3W9I-7 (WEB ONLY),   2012 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201302219933581817
  • ヒト脂肪由来間葉系幹細胞の再生医療への応用に向けた新規tet‐off制御型レンチウイルスベクターの構築, 椹木佳, 森山麻里子, 松山晃文, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 35th, 3P-0580 (WEB ONLY),   2012 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201302231421815697
  • 酸化ストレスを負荷したヒト脂肪組織由来新規多能性細胞によるPC12細胞の神経伸張誘導機序の解明, 森山博由, 森山麻里子, 松山晃文, 早川堯夫, 日本分子生物学会年会プログラム・要旨集(Web), 35th, 4P-0430 (WEB ONLY),   2012 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201302246760762389
  • 糖鎖を指標とする細胞評価法―再生医療実用化に向けた基礎検討―, 仲西暁良, 佐藤葵, 木下充弘, 森山博由, 早川堯夫, 掛樋一晃, 日本薬学会年会要旨集, 131年会, 3, 108, 108,   2011 03 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201102211223567976
  • 家族性高コレステロール血症ホモ接合体に対するin situ stem cell therapy in combinationの確立, 大倉華雪, 嵯峨礼美, 添田麻由美, 文元雄一, 森山麻里子, 森山博由, 永井宏治, 山下静也, 一瀬晃洋, 早川堯夫, 松山晃文, 再生医療, 10, 216,   2011 02 01 , http://jglobal.jst.go.jp/public/201102206233012677
  • 低酸素下におけるNotchシグナルの解糖系亢進作用への影響, 一志春樹, 森山麻里子, 大倉華雪, 松山晃文, 早川堯夫, 森山博由, 日本分子生物学会年会プログラム・要旨集(Web), 34th, 1P-0287 (WEB ONLY),   2011 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201202243460715463
  • キャピラリー電気泳動を用いる糖鎖を指標とする細胞評価法―再生医療実用化に向けた基礎検討―, 仲西暁良, 佐藤葵, 木下充弘, 森山博由, 早川堯夫, 掛樋一晃, キャピラリー電気泳動シンポジウム講演要旨集, 30th, 71, 72,   2010 11 15 , https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201102231646108391
  • Analysis of recombination site of HIV-1 sub type A/G recombinant.( Sponsor : Ministry of Health and Welfare )., 速水正憲, 井戸栄治, 森山博由, 武久盾, ビカンド ブレイス, ブジェカ イノサン, HIV感染症の疫学研究 平成9年度 研究報告書 HIV感染症の疫学研究班報告書, 444, 448,   1998 , http://jglobal.jst.go.jp/public/200902163989592112
  • 【COVID-19】(【COVID-19】SARS-CoV-2 infection among returnees on charter flights to Japan from Hubei, China: a report from National Center for Global Health and Medicine), Hayakawa Kayoko, Kutsuna Satoshi, Kawamata Takeo, Sugiki Yuko, Nonaka Chiharu, Tanaka Keiko, Shoji Michi, Nagai Masaki, Tezuka Shunsuke, Shinya Kazuyuki, Saito Hiroki, Harada Takahiro, Moriya Nin, Tsuboi Motoyuki, Norizuki Masataro, Sugiura Yasuo, Osanai Yasuyo, Sugiyama Masaya, Okuhama Ayako, Kanda Kohei, Wakimoto Yuji, Ujiie Mugen, Morioka Shinichiro, Yamamoto Kei, Kinoshita Noriko, Ishikane Masahiro, Saito Sho, Moriyama Yuki, Ota Masayuki, Nakamura Keiji, Nakamoto Takato, Ide Satoshi, Nomoto Hidetoshi, Akiyama Yutaro, Suzuki Tetsuya, Miyazato Yusuke, Gu Yoshiaki, Matsunaga Nobuaki, Tsuzuki Shinya, Fujitomo Yumiko, Kusama Yoshiki, Shichino Hiroyuki, Kaneshige Masao, Yamanaka Junko, Saito Miki, Hojo Masayuki, Hashimoto Masao, Izumi Shinyu, Takasaki Jin, Suzuki Manabu, Sakamoto Keita, Hiroi Yukio, Emoto Sakurako, Tokuhara Makoto, Kobayashi Toshiaki, Tomiyama Koichiro, Nakamura Fumihiko, Ohmagari Norio, Sugiyama Haruhito, Global Health & Medicine, 2, 2, 107, 111,   2020 04
  • FoxO3aはミトコンドリアダイナミクスの調節により創傷治癒に寄与する(FoxO3a plays roles in the wound healing by regulating mitochondrial dynamics), Moriyama Mariko, Kiriyama Hiroki, Hayakawa Takao, Moriyama Hiroyuki, 日本研究皮膚科学会年次学術大会・総会プログラム, 44回, 233, 233,   2019 10
  • 脂肪由来間質/幹細胞は表皮の恒常性を改善する(Adipose-derived stromal/stem cells improve epidermal homeostasis), Kiriyama Hiroki, Moriyama Mariko, Sahara Shunya, Zaiki Kaori, Ueno Ayumi, Nakaoji Koihi, Hamada Kazuhiko, Ozawa Toshiyuki, Tsuruta Daisuke, Hayakawa Takao, Moriyama Hiroyuki, 日本研究皮膚科学会年次学術大会・総会プログラム, 44回, 237, 237,   2019 10
  • 「エビデンスに基づくCKD診療ガイドライン2018」の要点(Essential points from Evidence-based Clinical Practice Guidelines for Chronic Kidney Disease 2018), Okada Hirokazu, Yasuda Yoshinari, Kashihara Naoki, Asahi Koichi, Ito Takafumi, Kaname Shinya, Kanda Eiichiro, Kanno Yoshihiko, Shikata Kenichi, Shibagaki Yugo, Tsuchiya Ken, Tsuruya Kazuhiko, Nagata Daisuke, Narita Ichiei, Nangaku Masaomi, Hattori Motoshi, Hamano Takayuki, Fujimoto Shouichi, Moriyama Toshiki, Yamagata Kunihiro, Yamamoto Ryohei, Wakasugi Minako, Ashida Akira, Usui Joichi, Kawamura Kazuko, Kitamura Kenichiro, Konta Tsuneo, Suzuki Yusuke, Tsuruoka Shuichi, Nishio Saori, Fujii Naohiko, Fujii Hideki, Wada Takehiko, Yokoyama Hitoshi, Aoki Katsunori, Akiyama Daiichiro, Araki Shin-ichi, Arima Hisatomi, Ishikawa Eiji, Ishikura Kenji, Ishizuka Kiyonobu, Ishimoto Takuji, Ishimoto Yu, Iseki Kunitoshi, Itabashi Mitsuyo, Ichioka Satoko, Ichikawa Kazunobu, Ichikawa Daisuke, Inoue Shuji, Imai Toshimi, Imamura Hideaki, Iwata Yasunori, Iwazu Yoshitaka, Usui Toshiaki, Uchida Keiko, Egawa Masahiro, Ohara Shinichiro, Omori Norio, Okada Rieko, Okuda Yusuke, Ozeki Takaya, Obata Yoko, Kai Hirayasu, Kato Noritoshi, Kanasaki Keizo, Kaneko Yoshikatsu, Kabasawa Hideyuki, Kawaguchi Takehiko, Kawasaki Yukihiko, Kawashima Keisuke, Kawano Haruna, Kikuchi Kan, Kihara Masao, Kimura Yoshiki, Kurita Noriaki, Koike Kentaro, Koizumi Masahiro, Kojima Chiari, Goto Shunsuke, Konomoto Takao, Kohagura Kentaro, Komatsu Hiroyuki, Komaba Hirotaka, Saito Chie, Sakai Yukinao, Sakaguchi Yusuke, Satonaka Hiroshi, Jimi Kanako, Shimizu Akihiro, Shimizu Sayaka, Shirai Sayuri, Shinzawa Maki, Sugiyama Kazuhiro, Suzuki Tomo, Suzuki Hitoshi, Suyama Kazuhide, Segawa Hiroyoshi, Takahashi Kazuya, Tanaka Kenichi, Tanaka Tetsuhiro, Tsunoda Ryoya, Tsuruta Yuki, Nakakura Hyogo, Nagasawa Yasuyuki, Nakanishi Koichi, Nagahama Masahiko, Nakaya Izaya, Nanami Masayoshi, Niihata Kakuya, Nishi Shinichi, Nishiwaki Hiroki, Hasegawa Shoko, Hasegawa Midori, Hanada Ken, Hayashi Hiroki, Harada Ryoko, Hishida Manabu, Hirano Daishi, Hirahashi Junichi, Hirama Akio, Hirayama Kouichi, Fukagawa Masafumi, Fukuda Akihiro, Fujii Yoshiyuki, Fujisaki Kiichiro, Furuya Fumihiko, Hoshino Junichi, Hosojima Michihiro, Honda Kenjiro, Masuda Takahiro, Matsui Kosuke, Matsukuma Yuta, Matsumura Hideki, Mii Akiko, Miura Kenichiro, Mitobe Michihiro, Miyasato Yoshikazu, Miyamoto Satoshi, Miwa Saori, Yazawa Masahiko, Yata Yusuke, Yamamoto Yoshihiro, Watanabe Kimio, Japanese Society of Nephrology, Committee of Evidence-based Practice Guideline for the Treatment of CKD 2018, Evidence-based Practice Guideline for the Treatment of CKD Production Group(Work group), Clinical and Experimental Nephrology, 23, 1, 1, 15,   2019 01
  • 急性腎障害診療ガイドライン2016日本語版(The Japanese Clinical Practice Guideline for acute kidney injury 2016), Doi Kent, Nishida Osamu, Shigematsu Takashi, Sadahiro Tomohito, Itami Noritomo, Iseki Kunitoshi, Yuzawa Yukio, Okada Hirokazu, Koya Daisuke, Kiyomoto Hideyasu, Shibagaki Yugo, Matsuda Kenichi, Kato Akihiko, Hayashi Terumasa, Ogawa Tomonari, Tsukamoto Tatsuo, Noiri Eisei, Negi Shigeo, Kamei Koichi, Kitayama Hirotsugu, Kashihara Naoki, Moriyama Toshiki, Terada Yoshio, Mori Kiyoshi, Taniyama Yoshihiro, Wakino Shu, Yasuda Hideo, Kume Shinji, Sofue Tadashi, Fujisaki Kiichiro, Shima Hideaki, Tomori Koji, Horino Taro, Watanabe Yusuke, Hayashi Hiroki, Moriguchi Takeshi, Yamashita Kazuto, Inokuchi Ryota, Nakamura Kensuke, Hara Yoshitaka, Furuichi Kengo, Sasaki Sho, Tsuji Takayuki, Yamada Hiroyuki, Yonemoto Sayoko, Nakada Taka-aki, Hattori Noriyuki, Yamashita Tetsushi, Kiuchi Zentaro, Sawada Mariko, Takahashi Masaki, Tani Masanori, Nakazawa Yusuke, Nunoyama Masaki, Fukui Tsuguya, Matsuo Seiichi, Maruyama Shoichi, Yanagita Motoko, Tsuruya Kazuhiko, The Japanese Clinical Practice Guideline for Acute Kidney Injury 2016 Committee, Journal of Intensive Care, 6, August, 1, 55,   2018 08
  • 日本人の黄斑色素密度の測定に用いられる市販の異色フリッカー光度計MPS2の信頼性(Reliability of a commercially available heterochromatic flicker photometer, the MPS2, for measuring the macular pigment optical density of a Japanese population), Obana Akira, Gohto Yuko, Moriyama Takatoshi, Seto Takahiko, Sasano Hiroyuki, Okazaki Shigetoshi, Japanese Journal of Ophthalmology, 62, 4, 473, 480,   2018 07
    Summary:日本人健常者24名(男性13名、女性11名、平均38.6歳)を対象に、黄斑色素密度(MPOD)の測定に用いられる異色フリッカー光度計Macular Pigment Screener(MPS2)の信頼性について検討した。MPS2とMacular Metrics II(MM2)で得られたMPODの一致度、試験-再試験信頼性を評価した。最終的にMPODの測定が可能であったのは、MPS2が23名、MM2が22名であった。検討の結果、MPS2を用いた場合の推定MPODは最小値0.24、最大値0.96、平均0.64、絶対MPODは最小値0.26、最大値0.94、平均0.63、MM2によるMPODは最小値0.29、最大値1.13、平均0.72であり、推定MPODと絶対MPODとの間に有意差は認められず、Pearsonの相関係数は0.82であった。MPS2で得られた絶対MPODの方がMM2でのMPODより有意に低値を示しており、相関係数は0.79であった。また、MPS2を用いたMPODの測定は5回実施し、級内相関係数は推定MPODが0.87、絶対MPODが0.80といずれも良好な成績であった。右眼と左眼のMPODに関して、MPS2でもMM2でも有意差はなく、MPS2を用いて測定した絶対MPODの方がMM2での測定値より有意に低値であった。日本人の黄斑色素密度の測定に際して、MPS2の信頼性は良好であったが、MM2と比較して有意に低値を示す傾向にあり、両者に互換性はないものと考えられた。
  • ヒト人工多能性幹細胞由来心筋を用いた不整脈誘発リスクの予測(Proarrhythmia risk prediction using human induced pluripotent stem cell-derived cardiomyocytes), Yamazaki Daiju, Kitaguchi Takashi, Ishimura Masakazu, Taniguchi Tomohiko, Yamanishi Atsuhiro, Saji Daisuke, Takahashi Etsushi, Oguchi Masao, Moriyama Yuta, Maeda Sanae, Miyamoto Kaori, Morimura Kaoru, Ohnaka Hiroki, Tashibu Hiroyuki, Sekino Yuko, Miyamoto Norimasa, Kanda Yasunari, Journal of Pharmacological Sciences, 136, 4, 249, 256,   2018 04
    Summary:ヒト人工多能性幹細胞由来心筋細胞(CM)のCor.4U-CMを用いて、微小電極アレイ(MEA)試験による不整脈誘発リスクの予測可能性を評価した。その結果、MEA法ではスパイク間隔とフィールド電位間隔(FPD)の間に線形回帰を認め、ヒトERG阻害薬のE-4031が逆使用依存性のFPD延長を誘導した。次に2次元マップを用いて不整脈誘発リスク予測を評価した。相対的torsade de pointes(TdP)リスクスコアはFridericia補正式変化によるFPDの程度と早期後脱分極の発生に基づいて決定し、血漿中有効治療濃度に規格化した薬剤のマージンを算出した。2次元マップを用いて薬剤を3種類のリスク群に分類した。その結果、このリスク分類法は公表されているデータベース、CredibleMedsから得たTdPリスク情報と良く一致した。以上より、Cor.4U-CMは薬物誘導性不整脈リスクの予測に用いることができると考えられた。
  • Sirt1は膜脂肪酸組成を改善し、ERストレス様反応を生じさせて心臓脂肪毒性を中和する(Sirt1 Counteracts Cardiac Lipotoxicity via Improving Membrane Fatty Acid Composition and Resulting ER Stress-Like Response), Yamamoto Tsunehisa, Endo Jin, Kataoka Masaharu, Matsuhashi Tomohiro, Katsumata Yoshinori, Shirakawa Kohsuke, Yoshida Naohiro, Isobe Sarasa, Moriyama Hidenori, Goto Shinichi, Yamashita Kaoru, Kono Nozomu, Arai Hiroyuki, Shinmura Ken, Fukuda Keiichi, Sano Motoaki, 日本循環器学会学術集会抄録集, 82回, YIA, 4,   2018 03
  • 表皮恒常性の維持におけるBNIP3誘発性自食作用の役割(Roles of BNIP3-induced autophagy in the maintenance of epidermal homeostasis), Moriyama Mariko, Morita Takashi, Marutani Yuuki, Uda Junki, Kubo Hirokazu, Hayakawa Takao, Moriyama Hiroyuki, 日本研究皮膚科学会年次学術大会・総会プログラム, 42回, 220, 220,   2017 11
  • アロエベラのゲルがヒト表皮に及ぼす創傷治癒作用の機序(Mechanism of Aloe vera gel on wound healing in human epidermis), Moriyama Mariko, Kubo Hirokazu, Nakajima Yuka, Goto Arisa, Akaki Junji, Yoshida Ikuyo, Nakamura Yukio, Hayakawa Takao, Moriyama Hiroyuki, 日本研究皮膚科学会年次学術大会・総会プログラム, 40回, 184, 184,   2015 11
  • 表皮角化細胞の分化と維持におけるBNIP3の必須の役割(BNIP3 PLAYS CRUCIAL ROLES IN THE DIFFERENTIATION AND MAINTENANCE OF EPIDERMAL KERATINOCYTES), Kubo Hirokazu, Moriyama Mariko, Nakajima Yuka, Goto Arisa, Hayakawa Takao, Moriyama Hiroyuki, 日本研究皮膚科学会年次学術大会・総会プログラム, 40回, 185, 185,   2015 11
  • BNIP3は表皮ケラチノサイトの分化と維持において必須の役割を果たす(BNIP3 plays crucial roles in the differentiation and maintenance of epidermal keratinocytes), Moriyama Mariko, Uda Junki, Moriyama Hiroyuki, Hayakawa Takao, 日本研究皮膚科学会年次学術大会・総会プログラム, 39回, 153, 153,   2014 11
  • TRANSPLANTATION OF HUMAN ADIPOSE TISSUE-DERIVED MULTILINEAGE PROGENITOR CELLS BUT NOT ADIPOSE TISSUE-DERIVED STROMAL/STEM CELLS REDUCES SERUM CHOLESTEROL IN HYPERLIPIDEMIC WATANABE RABBITS, H. Okura, M. Soeda, M. Morita, M. Moriyama, H. Moriyama, S. Yamashita, T. Hayakawa, A. Ichinose, A. Matsuyama, CARDIOLOGY, 126, 365, 365,   2013
  • TRANSPLANTATION OF ADIPOSE TISSUE-DERIVED MULTI-LINEAGE PROGENITOR CELLS REDUCES SERUM CHOLESTEROL IN HYPERLIPIDEMIC WATANABE RABBITS, M. Soeda, H. Okura, M. Morita, M. Moriyama, H. Moriyama, Y. Shizuya, T. Hayakawa, A. Ichinose, A. Matsuyama, CARDIOLOGY, 126, 292, 292,   2013
  • 表皮ケラチノサイトの分化および維持におけるオートファジー誘導因子BNIP3の重要な役割(Indispensable roles of BNIP3, an inducer of autophagy, in both differentiation and maintenance of epidermal keratinocytes), Moriyama Mariko, Uda Junki, Matsuyama Akifumi, Moriyama Hiroyuki, 日本研究皮膚科学会年次学術大会・総会プログラム, 37回, 169, 169,   2012 11
  • Breast tumor progression induced by loss of BTG2 expression is inhibited by targeted therapy with the ErbB/HER inhibitor lapatinib, F. Takahashi, N. Chiba, K. Tajima, T. Hayashida, T. Shimada, M. Takahashi, H. Moriyama, E. Brachtel, E. J. Edelman, S. Ramaswamy, S. Maheswaran, ONCOGENE, 30, 27, 3084, 3095,   2011 07 , 10.1038/onc.2011.24, https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79960048046&origin=inward
    Summary:The B-cell translocation gene-2 (BTG2), a p53-inducible gene, is suppressed in mammary epithelial cells during gestation and lactation. In human breast cancer, decreased BTG2 expression correlates with high tumor grade and size, p53 status, blood and lymph vessel invasion, local and metastatic recurrence and decrease in overall survival, suggesting that suppression of BTG2 has a critical role in disease progression. To analyze the role of BTG2 in breast cancer progression, BTG2 expression was knocked down in mammary epithelial cells. Suppression of BTG2 enhances the motility of cells in vitro and tumor growth and metastasis in vivo. The effects of BTG2 knockdown are mediated through stabilization of the human epidermal growth factor receptor (HER) ligands neuregulin and epiregulin and activation of the HER2 and HER3 receptors, leading to elevated AKT phosphorylation. Suppression of HER activation using the tyrosine kinase inhibitor lapatinib abrogates the effects of BTG2 knockdown, including the increased cell migration observed in vitro and the enhancement of tumorigenesis and metastasis in vivo. These results link BTG2-dependent effects on tumor progression to ErbB receptor signaling, and raise the possibility that targeted inhibition of this pathway may be relevant in the treatment of breast cancers that have reduced BTG2 expression. Oncogene (2011) 30, 3084-3095; doi: 10.1038/onc.2011.24; published online 21 February 2011