Details of the Researcher

PHOTO

Hiroshi Tawarayama
Section
Graduate School of Medicine
Job title
Assistant Professor
Degree

  • Ph.D. (Tohoku University)

e-Rad No.
20402414

Research Areas 1

  • Life sciences / Neuroscience - general /

Papers 30

  1. Mitochondrial cysteinyl-tRNA synthetase 2 protects against excitotoxic retinal cell death via enhanced supersulfide production Peer-reviewed

    Yuri Chida, Risa Shiokawa, Hiroshi Tawarayama, Minami Takeda, Hirokazu Hasegawa, Naoki Takahashi, Hiroshi Kunikata, Takaaki Akaike, Toru Nakazawa

    Free Radical Biology and Medicine　246　69-79　2026/03

    Publisher: Elsevier BV

    DOI： 10.1016/j.freeradbiomed.2026.01.009 　

    ISSN： 0891-5849

  2. 酸化ストレス負荷に対するエノラーゼ1の網膜神経保護効果の検討

    高橋 直樹, 俵山 寛司, 佐藤 孝太, 津田 聡, 中澤 徹

    日本緑内障学会抄録集　36回　88-88　2025/09

    Publisher: 日本緑内障学会

  3. Involvement of Microglia in Retinal Ganglion Cell Injury Induced by IOP Elevation in a Rat Ex Vivo Acute Glaucoma Model

    Taimu Sato, Makoto Ishikawa, Yukitoshi Izumi, Naoya Shibata, Kota Sato, Michiko Ohno-Oishi, Hiroshi Tawarayama, Hiroshi Kunikata, Charles F. Zorumski, Toru Nakazawa

    Biomedicines　2025/07/08

    DOI： 10.3390/biomedicines13071670 　

  4. ENO1 Dysfunction-Mediated Glycolytic Attenuation Exacerbates Oxidative Stress-Induced Retinal Ganglion Cell Death via Altered ATP Synthesis Pathway. International-journal Peer-reviewed

    Naoki Takahashi, Hiroshi Tawarayama, Yuri Chida, Minami Takeda, Risa Shiokawa, Kota Sato, Satoru Tsuda, Toru Nakazawa

    Investigative ophthalmology & visual science　66　(9)　63-63　2025/07/01

    DOI： 10.1167/iovs.66.9.63 　

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    PURPOSE: The effects of enolase dysfunction-mediated glycolytic attenuation on oxidative stress-induced retinal ganglion cell (RGC) death were investigated. METHODS: Retinal expression of Enolase (ENO) 1 and 2 was detected using immunohistochemistry. Exogenous genes were introduced into mouse RGCs using viral vectors, and into the rat-derived retinal progenitor cell line R28 using lipofection. The effects of enolase dysfunction were evaluated using N-methyl-D-aspartate (NMDA)-induced RGC death and H2O2-induced death assays. Cell viability and gene expression were investigated using the alamarBlue, quantitative RT-PCR, and Western blotting, respectively. Reactive oxygen species (ROS) were detected using CM-H2DCFDA dye. 2-deoxyglucose and oligomycin were used to attenuate adenosine triphosphate (ATP) production in glycolysis and oxidative phosphorylation (OXPHOS), respectively. RESULTS: ENO1 and ENO2 were expressed in the RGCs. Enolase overexpression inhibited NMDA-induced mouse RGC death, whereas deficiency of ENO1 but not ENO2 enhanced cell death. Additionally, ENO1 overexpression prevented the CDKN2B-induced enhancement of RGC death. H2O2 treatment increased ENO1 expression in R28 cells and inhibited H2O2-induced cell death. ATP production was immediately enhanced in ENO1 wild-type cells treated with H2O2. 2-deoxyglucose and oligomycin prevented enhanced ATP production, but ATP levels were still higher than, or similar to, those in untreated wild-type cells; in contrast, in knockdown cells, oligomycin-mediated OXPHOS inhibition led to lower ATP production in H2O2-treatment than in untreated cells. H2O2 treatment increased ROS production in knockdown R28 cells. CONCLUSIONS: ENO1 dysfunction leads to glycolytic attenuation, resulting in an excessive dependence of ATP production on OXPHOS under oxidative stress, contributing to excitotoxicity-induced RGC death. Preventing glycolytic attenuation may represent a promising treatment for RGC degeneration.

  5. Estrogen, via ESR2 receptor, prevents oxidative stress-induced Müller cell death and stimulates FGF2 production independently of NRF2, attenuating retinal degeneration Peer-reviewed

    Hiroshi Tawarayama, Keiko Uchida, Hirokazu Hasegawa, Masaaki Yoshida, Maki Inoue-Yanagimachi, Wataru Sato, Noriko Himori, Masayuki Yamamoto, Toru Nakazawa

    Experimental Eye Research　248　2024/11

    DOI： 10.1016/j.exer.2024.110103 　

    ISSN： 0014-4835

    eISSN： 1096-0007

  6. Nrf2欠損Mueller細胞はエストロゲン受容体β発現上昇を介して抗炎症効果が増強する

    内田 惠子, 檜森 紀子, 吉田 真彰, 俵山 寛司, 佐藤 孝太, 中澤 徹

    日本眼科学会雑誌　128　(臨増)　204-204　2024/03

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

  7. Glutathione trisulfide prevents lipopolysaccharide-induced retinal inflammation via inhibition of proinflammatory cytokine production in glial cells. International-journal Peer-reviewed

    Hiroshi Tawarayama, Kota Umeki, Maki Inoue-Yanagimachi, Naoki Takahashi, Hirokazu Hasegawa, Noriko Himori, Satoru Tsuda, Hiroshi Kunikata, Takaaki Akaike, Toru Nakazawa

    Scientific reports　13　(1)　11513-11513　2023/07/17

    DOI： 10.1038/s41598-023-38696-4 　

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    We aimed to investigate the impact of glutathione trisulfide (GSSSG) on lipopolysaccharide (LPS)-induced inflammation in retinal glia. Inflammatory responses in mouse-derived glial cells and Wistar rat retinas were stimulated with administration of LPS. Cell survival and proinflammatory cytokine production were examined using the Calcein-AM assay, and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Retinal microglia were visualized with immunohistochemistry for Iba1. Administration of LPS (10 µg/mL) or GSSSG (less than 100 µM) did not affect survival of cultured primary Müller cells and established microglial cells (BV-2). RT-qPCR and ELISA indicated that GSSSG inhibited LPS-induced gene upregulation and protein secretion of proinflammatory cytokines in these glial cells and rat retinas. GSSSG inhibited LPS-induced activation of TGF-β-activated kinase 1 (TAK1), which is an upstream kinase of NF-κB, in BV-2 cells. Finally, in vivo experiments indicated that intravitreal administration of GSSSG but not its relative glutathione disulfide (GSSG) inhibited LPS (500 ng)-induced accumulation of Iba1-immunopositive microglia in rat retinas. Taken together, GSSSG has the potential to prevent pathogenesis of inflammation-associated ocular diseases by inhibiting proinflammatory cytokine expression in retinal glial cells.

  8. Isozyme-specific Histone Deacetylase 1/2 Inhibitor K560 Attenuates Oxidative Stress-induced Retinal Cell Death. International-journal Peer-reviewed

    Hiroshi Tawarayama, Yoshiyuki Hirata, Uchida Keiko, Noriko Himori, Shinichi Uesato, Toru Nakazawa

    Neuroscience letters　793　136978-136978　2022/11/23

    DOI： 10.1016/j.neulet.2022.136978 　

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    Oxidative stress-induced damage is an underlying mechanism in the pathogenesis of age-related retinal diseases. Here, we examined the effects of K560, a potential candidate drug for the treatment of these diseases, on oxidative stress-induced retinal cell death. K560 is a novel isozyme-specific inhibitor of histone deacetylase 1 and 2 (HDAC1/2). Histone acetylation in retinal lysates and dissociated retinal cells was detected with a western blot analysis and cell-based enzyme-linked immunosorbent assay (ELISA), respectively. The viability of mouse retinal cells was measured with an alamarBlue assay. We used immunohistochemistry for RNA binding protein with multiple splicing (RBPMS) to visualize the retinal ganglion cells (RGCs) of mice. A ELISA analysis indicated that histone acetylation was enhanced in dissociated mouse retinal cells tretaed with K560. The cell viability assay indicated that K560 attenuated both exogenous hydrogen peroxide-induced and endogenous oxidative stress-induced cell death in dissociated retinal cells. Western blot analysis indicated that intravitreal K560 administration enhanced the acetylation of histones H3 and H4 in mouse retinal lysates. To examine the effect of K560 on oxidative stress-induced RGC death, we performed whole-mount immunohistochemistry for RBPMS for retinas dissected from eyes treated with K560 or vehicle on day one, and K560 or vehicle and NMDA on day two. Quantification of RBPMS-immunopositive cells indicated that K560 attenuated NMDA-induced RGC death. Taken together, our findings suggest that administration of a HDAC1/2-specific inhibitor, i.e., K560, may be effective in the treatment of oxidative stress-mediated retinal degeneration and have less cytotoxicity than other known HDAC inhibitors, which are known to target a wide range of HDAC family members.

  9. Changes in glial cells and neurotrophic factors due to rotenone-induced oxidative stress in Nrf2 knockout mice. International-journal Peer-reviewed

    Maki Inoue-Yanagimachi, Noriko Himori, Keiko Uchida, Hiroshi Tawarayama, Kota Sato, Masayuki Yamamoto, Kazuhiko Namekata, Takayuki Harada, Toru Nakazawa

    Experimental eye research　226　109314-109314　2022/11/15

    DOI： 10.1016/j.exer.2022.109314 　

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    Glaucoma is one of the most common causes of blindness worldwide. It is thought to be a multifactorial disease with underlying mechanisms that include mitochondrial dysfunction and oxidative stress. Here, we used NF-E2 related factor 2 (Nrf2) knockout (KO) mice, which are vulnerable to oxidative stress, to examine a neuroprotective effect against oxidative stress due to rotenone, a mitochondrial complex I inhibitor. Wild-type (WT) and Nrf2 KO mice received an oral solution of rotenone for 30 days. We then extracted the retinas and performed immunohistochemistry and quantitative RT-PCR. We also prepared a primary Müller cell culture of samples from each mouse, added 30 μM rotenone, and then measured cell viability, cytotoxicity and CellRox absorbance. We also examined gene expression. We found a significant increase in the number of 8-OHdG-positive retinal ganglion cells (RGCs) after rotenone administration in both the WT and Nrf2 KO mice. There was no difference in the number of RNA-binding protein with multiple splicing (RBPMS)-positive RGCs in the WT and Nrf2 KO mice, but Nrf2 KO mice that were given rotenone had significantly less retinal gene expression of RBPMS than Nrf2 KO mice given a control. Moreover, there was significantly higher mRNA gene expression of vimentin and glial fibrillary acidic protein (GFAP) in Nrf2 KO mice that received rotenone than WT mice that received rotenone. A statistical analysis of the in vitro experiment showed that cell viability was lower, cytotoxicity was higher, and oxidative stress was higher in the Müller cells of the Nrf2 KO mice than the WT mice. Finally, brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor (bFGF) were significantly higher in the Müller cells of the Nrf2 KO mice than the WT mice. These findings suggest that in Nrf2 KO mice under oxidative stress caused by rotenone, temporary neurotrophic factors are secreted from the Müller cells, conferring neuroprotection in these cells.

  10. Development of an anti-oxidative intraocular irrigating solution based on reactive persulfides. International-journal Peer-reviewed

    Hiroshi Kunikata, Hiroshi Tawarayama, Satoru Tsuda, Takaaki Akaike, Toru Nakazawa

    Scientific reports　12　(1)　19243-19243　2022/11/10

    DOI： 10.1038/s41598-022-21677-4 　

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    Anti-oxidative intraocular irrigating solutions (IISs) based on reactive persulfides, such as oxidized glutathione disulfide (GSSG), are commonly used worldwide. However, even with GSSG-based IISs, it has been shown that oxidative stress can occur during surgery, posing a risk to intraocular tissues. This study compared two IISs: one containing GSSG and one containing an oxidized glutathione trisulfide (GSSSG). Experimental in vivo irrigation with the IISs in rabbits showed that there was less leakage into the anterior chamber of rabbit serum albumin during perfusion with a 300-μM GSSSG IIS than with a 300-μM GSSG IIS. Experimental in vivo cataract surgery in rabbits showed that aqueous flare was suppressed 3 days after surgery with a 600-μM GSSSG IIS, but not with a 300-μM GSSSG or 300-μM GSSG IIS. Furthermore, an in vitro experiment, without any live tissue, showed that reactive oxygen species were suppressed more strongly with a 600-μM GSSSG IIS than with a 300-μM GSSG IIS. Thus, this study found that novel IISs based on GSSSG had anti-inflammatory and anti-oxidative effects during and after intraocular surgery and may decrease the rate of complications after surgery.

  11. ロテノン誘導性酸化ストレス負荷環境下におけるグリア細胞分泌物の役割

    柳町 真希, 俵山 寛司, 檜森 紀子, 中澤 徹

    日本緑内障学会抄録集　33回　81-81　2022/09

    Publisher: 日本緑内障学会

  12. Glutathione Trisulfide Prevents Lipopolysaccharide-induced Inflammatory Gene Expression in Retinal Pigment Epithelial Cells Peer-reviewed

    Hiroshi Tawarayama, Noriyuki Suzuki, Maki Inoue-Yanagimachi, Noriko Himori, Satoru Tsuda, Kota Sato, Tomoaki Ida, Takaaki Akaike, Hiroshi Kunikata, Toru Nakazawa

    Ocular Immunology and Inflammation　30　(4)　789-800　2022/05/19

    Publisher: Informa UK Limited

    DOI： 10.1080/09273948.2020.1833224 　

    ISSN： 0927-3948

    eISSN： 1744-5078

  13. Glial cells modulate retinal cell survival in rotenone-induced neural degeneration. International-journal Peer-reviewed

    Hiroshi Tawarayama, Maki Inoue-Yanagimachi, Noriko Himori, Toru Nakazawa

    Scientific reports　11　(1)　11159-11159　2021/05/27

    DOI： 10.1038/s41598-021-90604-w 　

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    Administration of the mitochondrial complex I inhibitor rotenone provides an excellent model to study the pathomechanism of oxidative stress-related neural degeneration diseases. In this study, we examined the glial roles in retinal cell survival and degeneration under the rotenone-induced oxidative stress condition. Mouse-derived Müller, microglial (BV-2), and dissociated retinal cells were used for in vitro experiments. Gene expression levels and cell viability were determined using quantitative reverse transcription-polymerase chain reaction and the alamarBlue assay, respectively. Conditioned media were prepared by stimulating glial cells with rotenone. Retinal ganglion cells (RGCs) and inner nuclear layer (INL) were visualized on rat retinal sections by immunohistochemistry and eosin/hematoxylin, respectively. Rotenone dose-dependently induced glial cell death. Treatment with rotenone or rotenone-stimulated glial cell-conditioned media altered gene expression of growth factors and inflammatory cytokines in glial cells. The viability of dissociated retinal cells significantly increased upon culturing in media conditioned with rotenone-stimulated or Müller cell-conditioned media-stimulated BV-2 cells. Furthermore, intravitreal neurotrophin-5 administration prevented the rotenone-induced reduction of RGC number and INL thickness in rats. Thus, glial cells exerted both positive and negative effects on retinal cell survival in rotenone-induced neural degeneration via altered expression of growth factors, especially upregulation of microglia-derived Ntf5, and proinflammatory cytokines.

  14. ミトコンドリアComplex I阻害時のマウスミュラー細胞における神経栄養因子の検討

    柳町 真希, 檜森 紀子, 俵山 寛司, 佐藤 孝太, 行方 和彦, 原田 高幸, 山本 雅之, 中澤 徹

    日本緑内障学会抄録集　31回　72-72　2020/10

    Publisher: 日本緑内障学会

  15. Draxin-mediated Regulation of Granule Cell Progenitor Differentiation in the Postnatal Hippocampal Dentate Gyrus International-journal Peer-reviewed

    Hiroshi Tawarayama, Hirohisa Yamada, Ruhul Amin, Yuiko Morita-Fujimura, Helen M Cooper, Yohei Shinmyo, Hideaki Tanaka, Shuntaro Ikawa

    Neuroscience　431　184-192　2020/04

    Publisher: Elsevier BV

    DOI： 10.1016/j.neuroscience.2020.02.005 　

    ISSN： 0306-4522

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    The hippocampus is characterized by the presence of life-long neurogenesis. To elucidate the molecular mechanism regulating hippocampal neurogenesis, we studied the functions of the chemorepellent Draxin in neuronal proliferation and differentiation in the postnatal dentate gyrus. The present in vivo cell labeling and fate tracking analyses revealed enhanced differentiation of hippocampal neural stem and progenitor cells (hNSPCs) in the subgranular zone (SGZ) of Draxin-deficient mice. We observed a reduction in the number of BrdU-pulse labeled or Ki-67 immunopositive SGZ cells in the mutant mice. However, Draxin deficiency did not affect cell cycle duration of SGZ cells. In situ hybridization analysis indicated that the receptor component of the canonical Wnt pathway, Lrp6, is expressed in SGZ cells, including Nestin and Sox2 double-positive hNSPCs. Taken together with the previous finding that Draxin interacts physically with Lrp6, we postulate that Draxin plays a pivotal role in the regulation of Wnt-driven hNSPC differentiation to modulate the rate of neuronal differentiation in the progenitor population.

  16. ウサギ模擬白内障手術を用いたグルタチオン三硫化物(GS3G)による眼組織保護効果の検討

    鈴木 哲章, 國方 彦志, 俵山 寛司, 佐藤 孝太, 津田 聡, 中澤 徹

    日本眼科学会雑誌　124　(臨増)　183-183　2020/03

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

  17. Cyclin-Dependent Kinase Inhibitor 2b Mediates Excitotoxicity-Induced Death of Retinal Ganglion Cells Peer-reviewed

    Hiroshi Tawarayama, Qiwei Feng, Namie Murayama, Noriyuki Suzuki, Toru Nakazawa

    Investigative Opthalmology & Visual Science　60　(13)　4479-4479　2019/10/01

    Publisher: Association for Research in Vision and Ophthalmology (ARVO)

    DOI： 10.1167/iovs.19-27396 　

    ISSN： 1552-5783

  18. Draxin regulates hippocampal neurogenesis in the postnatal dentate gyrus by inhibiting DCC-induced apoptosis Peer-reviewed

    Hiroshi Tawarayama, Hirohisa Yamada, Ruhul Amin, Yuiko Morita-Fujimura, Helen M. Cooper, Yohei Shinmyo, Masakado Kawata, Shuntaro Ikawa, Hideaki Tanaka

    Scientific Reports　8　(1)　840　2018/12/01

    Publisher: Nature Publishing Group

    DOI： 10.1038/s41598-018-19346-6 　

    ISSN： 2045-2322

  19. 【感覚器障害の治療と研究の最前線 QOL向上とコミュニケーションのあり方を考える】先進感覚器研究コアセンターの感覚器研究プロジェクト

    國方 彦志, 佐藤 孝太, 俵山 寛司, 中澤 徹

    ファルマシア　54　(11)　1025-1029　2018/11

    Publisher: (公社)日本薬学会

    ISSN： 0014-8601

    eISSN： 2189-7026

  20. Ecel1 Knockdown With an AAV2-Mediated CRISPR/Cas9 System Promotes Optic Nerve Damage-Induced RGC Death in the Mouse Retina Peer-reviewed

    Kota Sato, Yukihiro Shiga, Yurika Nakagawa, Kosuke Fujita, Koji M. Nishiguchi, Hiroshi Tawarayama, Namie Murayama, Shigeto Maekawa, Takeshi Yabana, Kazuko Omodaka, Shota Katayama, Qiwei Feng, Satoru Tsuda, Toru Nakazawa

    Investigative Opthalmology & Visual Science　59　(10)　3943-3943　2018/08/01

    Publisher: Association for Research in Vision and Ophthalmology (ARVO)

    DOI： 10.1167/iovs.18-23784 　

    ISSN： 1552-5783

  21. The chemorepellent draxin is involved in hippocampal mossy fiber projection Peer-reviewed

    Hiroshi Tawarayama, Hirohisa Yamada, Yohei Shinmyo, Hideaki Tanaka, Shuntaro Ikawa

    Biochemical and Biophysical Research Communications　500　(2)　217-223　2018/06/02

    Publisher: Elsevier B.V.

    DOI： 10.1016/j.bbrc.2018.04.043 　

    ISSN： 1090-2104 0006-291X

  22. Novel function of the chemorepellent draxin as a regulator for hippocampal neurogenesis Peer-reviewed

    Hiroshi Tawarayama

    Neural Regeneration Research　13　(5)　799-800　2018/05/01

    Publisher: Medknow Publications

    DOI： 10.4103/1673-5374.232465 　

    ISSN： 1876-7958 1673-5374

  23. The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation Peer-reviewed

    Shigeto Maekawa, Kota Sato, Kosuke Fujita, Reiko Daigaku, Hiroshi Tawarayama, Namie Murayama, Satoru Moritoh, Takeshi Yabana, Yukihiro Shiga, Kazuko Omodaka, Kazuichi Maruyama, Koji M. Nishiguchi, Toru Nakazawa

    Scientific Reports　7　(1)　6885　2017/12/01

    Publisher: Nature Publishing Group

    DOI： 10.1038/s41598-017-06969-4 　

    ISSN： 2045-2322

  24. Metabolomic profiling of reactive persulfides and polysulfides in the aqueous and vitreous humors Peer-reviewed

    Hiroshi Kunikata, Tomoaki Ida, Kota Sato, Naoko Aizawa, Tomohiro Sawa, Hiroshi Tawarayama, Namie Murayama, Shigemoto Fujii, Takaaki Akaike, Toru Nakazawa

    SCIENTIFIC REPORTS　7　41984　2017/02

    DOI： 10.1038/srep41984 　

    ISSN： 2045-2322

  25. Delta Np63 alpha induces quiescence and downregulates the BRCA1 pathway in estrogen receptor-positive luminal breast cancer cell line MCF7 but not in other breast cancer cell lines Peer-reviewed

    Ruhul Amin, Yuiko Morita-Fujimura, Hiroshi Tawarayama, Kentaro Semba, Natsuko Chiba, Manabu Fukumoto, Shuntaro Ikawa

    MOLECULAR ONCOLOGY　10　(4)　575-593　2016/04

    DOI： 10.1016/j.molonc.2015.11.009 　

    ISSN： 1574-7891

    eISSN： 1878-0261

  26. Roles of Semaphorin-6B and Plexin-A2 in Lamina-Restricted Projection of Hippocampal Mossy Fibers Peer-reviewed

    Hiroshi Tawarayama, Yutaka Yoshida, Fumikazu Suto, Kevin J. Mitchell, Hajime Fujisawa

    JOURNAL OF NEUROSCIENCE　30　(20)　7049-7060　2010/05

    DOI： 10.1523/JNEUROSCI.0073-10.2010 　

    ISSN： 0270-6474

  27. Sema3a1 guides spinal motor axons in a cell- and stage-specific manner in zebrafish Peer-reviewed

    Mika Sato-Maeda, Hiroshi Tawarayama, Masuo Obinata, John Y. Kuwada, Wataru Shoji

    Development　133　(5)　937-947　2006/03/01

    DOI： 10.1242/dev.02268 　

    ISSN： 0950-1991

    eISSN： 1477-9129

  28. Estrogen synthesis in relation to gonadal development of Japanese scallop, Patinopecten yessoensis: gonadal profile and immunolocalization of P450 aromatase and estrogen Peer-reviewed

    Makoto Osada, Hiroshi Tawarayama, Katsuyoshi Mori

    Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology　139　(1)　123-128　2004/09

    DOI： 10.1016/j.cbpc.2004.07.002 　

    ISSN： 1096-4959

  29. Repulsion and attraction of axons by Semaphorin3D are mediated by different neuropilins in vivo Peer-reviewed

    MA Wolman, Y Liu, H Tawarayama, W Shoji, MC Halloran

    JOURNAL OF NEUROSCIENCE　24　(39)　8428-8435　2004/09

    DOI： 10.1523/JNEUROSCI.2349-04.2004 　

    ISSN： 0270-6474

  30. Semaphorin3D guides retinal axons along the dorsoventral axis of the tectum. International-journal Peer-reviewed

    Yan Liu, Jason Berndt, Fengyun Su, Hiroshi Tawarayama, Wataru Shoji, John Y Kuwada, Mary C Halloran

    The Journal of neuroscience : the official journal of the Society for Neuroscience　24　(2)　310-8　2004/01/14

    DOI： 10.1523/jneurosci.4287-03.2004 　

    ISSN： 0270-6474

    eISSN： 1529-2401

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Misc. 4

  1. Enolase-Mediated Neuroprotection Against Excitotoxic Retinal Ganglion Cell Death

    高橋直樹, 俵山寛司, 佐藤孝太, 津田聡, 中澤徹

    日本眼科学会雑誌　129　2025

    ISSN： 0029-0203

  2. Changes in NLRP3 modulated by microglia in a rat ex vivo glaucoma model

    佐藤大夢, 石川誠, 大石路子, 神位りえ子, 佐藤孝太, 俵山寛司, 中澤徹

    日本眼科学会雑誌　128　2024

    ISSN： 0029-0203

  3. AAV2-CRISPR/Cas9システムを用いた網膜神経節細胞のゲノム編集

    佐藤孝太, 藤田幸輔, 俵山寛司, 片山翔太, 西口康二, 中澤徹

    日本眼科学会雑誌　123　2019

    ISSN： 0029-0203

  4. 先進感覚器研究コアセンターの感覚器研究プロジェクト

    國方彦志, 佐藤孝太, 俵山寛司, 中澤徹

    ファルマシア(Web)　54　(11)　1025‐1029(J‐STAGE)　2018

    DOI： 10.14894/faruawpsj.54.11_1025 　

    ISSN： 2189-7026

Research Projects 9

  1. 新規眼内炎症緩和剤として期待される活性イオウ分子種によるIL1B発現制御機序の解明

    俵山 寛司, 中澤 徹

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2024/04/01 - 2027/03/31

  2. GWASによる緑内障感受性遺伝子CDKN2B-AS1のメカニズム解明

    面高 宗子, 俵山 寛司, 中澤 徹

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2024/04/01 - 2027/03/31

  3. グルタチオン三硫化物GSSSGの抗酸化・抗炎症作用に基づく難治性眼疾患の病態制御

    國方 彦志, 俵山 寛司, 中澤 徹

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2023/04/01 - 2026/03/31

  4. STING経路に着目した滲出型加齢黄斑変性の網膜下線維化の病態解明

    安田 正幸, 俵山 寛司, 佐藤 孝太

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2023/04/01 - 2026/03/31

  5. 炎症性眼疾患の治療・緩和を見据えた活性イオウ分子種による抗炎症作用機序の解明

    俵山 寛司

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 基盤研究(C)

    Category: 基盤研究(C)

    Institution: 東北大学

    2021/04/01 - 2024/03/31

  6. Development of a HDAC1/2 inhibitor K560-mediated treatment for glaucoma Competitive

    Tawarayama Hiroshi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2018/04/01 - 2021/03/31

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    Retinal ganglion cell (RGC) death is the symptom of glaucoma. It is thought that oxidative stress partially contributes the cell death. In this study, we investigated the effect of K560, an isozyme selective inhibitor of histone deacetylase (HDAC) 1/2, on oxidative stress-induced RGC death, and found that (1) K560 attenuated oxidative stress-induced death of dissociated retinal cells in mice, (2) K560 enhanced histone acetylation of retinal lysates prepared from mice administered with K560 intravitreally, (3) K560 inhibited oxidative stress-induced RGC death in mice. These findings suggested that K560 administration is a promising treatment for glaucoma.

  7. The roles of the chamorepellent draxin in hippocampal neurogenesis Competitive

    Tawarayama Hiroshi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2015/10/21 - 2018/03/31

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    Hippocampal neurogenesis in the dentate gyrus (DG) is controlled by various diffusible molecules that modulate neurogenic processes. To elucidate the mechanisms underlying hippocampal neurogenesis, we investigated the function of draxin in the regulation of neuronal survival in the DG. Draxin was expressed in Tbr2 (+) late progenitors and NeuroD1 (+) neuroblasts in the dentate granule cell lineage, whereas expression of its receptor DCC was mainly detectable in neuroblasts. Our phenotypic analysis revealed that draxin deficiency led to enhanced apoptosis of DCC-expressing neuroblasts in the neurogenic areas. Furthermore, in vitro assays using a hippocampal neural stem/progenitor cell (HNSPC) line indicated that draxin inhibited apoptosis in differentiating HNSPCs, which express DCC. Taken together, we postulate that draxin plays a pivotal role in postnatal DG neurogenesis as a dependence receptor ligand for DCC to maintain and promote survival of neuroblasts.

  8. 癲癇モデルマウスを用いたタキシフェン 誘導 体リダイフェン-D による神経保護効果の検討 Competitive

    俵山 寛司

    Offer Organization: 東北大学

    System: 研究所若手アンサンブルグラント

    2015/04 - 2016/03

  9. Roles of draxin in hippocampal development as a neurotrophic factor Competitive

    TAWARAYAMA Hiroshi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)

    Category: Grant-in-Aid for Young Scientists (B)

    2013/04/01 - 2015/03/31

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    Granule cell production in the hippocampus dentate gyrus is fundamental to brain functions such as learning and memory. Although the previous study revealed that loss of draxin, which we previously identified as a neural repellent, leads to reduction in number of granule cells and hippocampal volume, little is known bout the mechanisms in which draxin regulates the hippocampal development. In this study, we report the dual role of draxin in hippocampal neurogenesis: (1) Draxin prevents the DCC-induced apoptosis of differentiating neurons by acting as a ligand for the dependence receptor, and promote neuronal survival through the receptors DCC and neogenin. (2) Draxin modulates differentiation of neuronal progenitors by attenuating the neuronal-differentiation-promoting activity of canonical Wnts. The draxin-mediated modulation would be useful for preventing depletion of progenitors, which vigorously proliferate, due to too rapid differentiation.

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