| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○招待 (推奨): |
| ○審査 (推奨): |
| ○カテゴリ (推奨): |
| ○共著種別 (推奨): | □ | 国内共著 (徳島大学内研究者と国内(学外)研究者との共同研究 (国外研究者を含まない))
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| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Akaiwa Kei (日) 赤岩 慶 (読) あかいわ けい
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| ○学籍番号 (推奨): | □ | ****
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| 2. | (英) Kazuhiko Namekata (日) (読)
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| 3. | (英) Yuriko Azuchi (日) (読)
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| ○学籍番号 (推奨): |
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| 4. | (英) Sano Hiroki (日) 佐埜 弘樹 (読) さの ひろき
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): | □ | ****
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| 5. | (英) Xiaoli Guo (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 6. | (英) Atsuko Kimura (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 7. | (英) Chikako Harada (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 8. | 三田村 佳典 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.外科系.眼科学])
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
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| 9. | (英) Takayuki Harada (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| ○題名 (必須): | □ | (英) Topical ripasudil suppresses retinal ganglion cell death in a mouse model of normal tension glaucoma (日)
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| ○副題 (任意): |
| ○要約 (任意): | □ | (英) To assess if ripasudil has a neuroprotective effect using mice with excitatory amino acid carrier 1 (EAAC1) deletion (EAAC1 knockout [KO] mice), a mouse model of normal tension glaucoma. Topical administration (5 μL/day) of two different concentrations of ripasudil (0.4% and 2%) were applied to EAAC1 KO mice from 5 to 12 weeks old. Optical coherence tomography, multifocal electroretinograms, the measurement of intraocular pressure (IOP), and histopathology analyses were performed at 5, 8, and 12 weeks old. Retrograde labeling of retinal ganglion cells (RGCs), immunoblot, and immunohistochemical analyses of phosphorylated p38 mitogen-activated protein kinase (MAPK) in the retina were performed at 8 weeks old. Topical ripasudil ameliorated retinal degeneration and improved visual function in EAAC1 KO mice at both 8 and 12 weeks old. Ripasudil reduced IOP and strongly suppressed the phosphorylation of p38 MAPK that stimulates RGC death in EAAC1 KO mice. These results suggest that, in addition to IOP reduction, ripasudil prevents glaucomatous retinal degeneration by neuroprotection, which is achieved by suppressing cell-death signaling pathways. (日)
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| ○キーワード (推奨): | 1. | (英) Administration, Ophthalmic (日) (読)
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| 2. | (英) Animals (日) (読)
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| 3. | (英) Cell Death (日) (読)
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| 4. | (英) Disease Models, Animal (日) (読)
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| 5. | (英) Electroretinography (日) (読)
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| 6. | (英) Excitatory Amino Acid Transporter 3 (日) (読)
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| 7. | (英) Immunoblotting (日) (読)
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| 8. | (英) Immunohistochemistry (日) (読)
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| 9. | (英) Intraocular Pressure (日) (読)
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| 10. | (英) Isoquinolines (日) (読)
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| 11. | (英) Low Tension Glaucoma (日) (読)
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| 12. | (英) Mice (日) (読)
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| 13. | (英) Mice, Inbred C57BL (日) (読)
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| 14. | (英) Mice, Knockout (日) (読)
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| 15. | (英) Phosphorylation (日) (読)
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| 16. | (英) Retinal Degeneration (日) (読)
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| 17. | (英) Retinal Ganglion Cells (日) (読)
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| 18. | (英) Sulfonamides (日) (読)
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| 19. | (英) Tomography, Optical Coherence (日) (読)
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| 20. | (英) Tonometry, Ocular (日) (読)
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| 21. | (英) p38 Mitogen-Activated Protein Kinases (日) (読)
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| 22. | (英) rho-Associated Kinases (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Investigative Ophthalmology & Visual Science (Association for Research in Vision and Ophthalmology)
(pISSN: 0146-0404, eISSN: 1552-5783)
| ○ISSN (任意): | □ | 1552-5783
ISSN: 0146-0404
(pISSN: 0146-0404, eISSN: 1552-5783) Title: Investigative ophthalmology & visual scienceTitle(ISO): Invest Ophthalmol Vis SciPublisher: Association for Research in Vision and Ophthalmology (NLM Catalog)
(Scopus)
(CrossRef)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 59
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| ○号 (必須): | □ | 5
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| ○頁 (必須): | □ | 2080 2089
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2018年 4月 1日 (平成 30年 4月 1日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1167/iovs.17-23276 (→Scopusで検索)
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| ○PMID (任意): | □ | 29677370 (→Scopusで検索)
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| ○CRID (任意): |
| ○WOS (任意): |
| ○Scopus (任意): | □ | 2-s2.0-85045733265
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| ○評価値 (任意): |
| ○被引用数 (任意): |
| ○指導教員 (推奨): |
| ○備考 (任意): | 1. | (英) Article.ELocationID: 10.1167/iovs.17-23276 (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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