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<Originals> c-Jun N-terminal kinase (JNK) mediates Rho/ROCK induced Sox9 diminution in chondrocytes
https://kindai.repo.nii.ac.jp/records/10566
https://kindai.repo.nii.ac.jp/records/10566176f0bd9-48fd-4899-99da-167f415c3a9b
| 名前 / ファイル | ライセンス | アクション |
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||||||||||||||
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| 公開日 | 2014-05-27 | |||||||||||||||||||||
| タイトル | ||||||||||||||||||||||
| タイトル | <Originals> c-Jun N-terminal kinase (JNK) mediates Rho/ROCK induced Sox9 diminution in chondrocytes | |||||||||||||||||||||
| 言語 | en | |||||||||||||||||||||
| 著者 |
Onodera, Yuta
× Onodera, Yuta
× Teramura, Takeshi
× Takehara, Toshiyuki
× Fukuda, Kanji
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| 言語 | ||||||||||||||||||||||
| 言語 | eng | |||||||||||||||||||||
| キーワード | ||||||||||||||||||||||
| 主題 | JNK, Rho/ROCK, chondrocyte, Sox9 | |||||||||||||||||||||
| 資源タイプ | ||||||||||||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||||||||||||||
| 資源タイプ | departmental bulletin paper | |||||||||||||||||||||
| 著者 所属 | ||||||||||||||||||||||
| 値 | Institute of Advanced Clinical Medicine | |||||||||||||||||||||
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| 値 | Institute of Advanced Clinical Medicine | |||||||||||||||||||||
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| 値 | Institute of Advanced Clinical Medicine | |||||||||||||||||||||
| 著者 所属 | ||||||||||||||||||||||
| 値 | Institute of Advanced Clinical Medicine, Department of Rehabilitation Medicine, Kinki University Faculty of Medicine | |||||||||||||||||||||
| 著者所属(翻訳) | ||||||||||||||||||||||
| 値 | Kinki University | |||||||||||||||||||||
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| 値 | Kinki University | |||||||||||||||||||||
| 著者所属(翻訳) | ||||||||||||||||||||||
| 値 | Kinki University | |||||||||||||||||||||
| 著者所属(翻訳) | ||||||||||||||||||||||
| 値 | Kinki University | |||||||||||||||||||||
| 版 | ||||||||||||||||||||||
| 出版タイプ | VoR | |||||||||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||||||||||||
| 出版者 名前 | ||||||||||||||||||||||
| 出版者 | Kinki University Medical Association | |||||||||||||||||||||
| 書誌情報 |
en : ACTA MEDICA KINKI UNIVERSITY 巻 38, 号 2, p. 91-100, 発行日 2013-12-01 |
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| 収録物識別子タイプ | ISSN | |||||||||||||||||||||
| 収録物識別子 | 03866092 | |||||||||||||||||||||
| 抄録 | ||||||||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||||||||
| 内容記述 | [Abstract] Objective Comprehensive molecular mechanisms connecting stress sensing to cellular phenotypic alteration is essential for developinga therapeutic strategy for osteoarthritis (OA). In recent studies, the possibility that small GTPase Rho families and its effector kinase ROCK (Rho/ROCK) could be a molecular switch in various stress-mediated signaling cascades was suggested, and is now gaining attention as a promising pharmacological target in various regions ; however, the relationship of Rho/ROCK to cartilage development and maintenance has not been well elucidated. Methods In this study, we used a mouse chondroprogenitor cell line ATDC5, bovine primary chondrocytes and human cultured articularchondrocytes. Rho activation was induced by administration of lysophosphatidic acid (LPA), which is a potent activator of Rho, or introduction of plasmids encoding dominant-active or negative RhoA. Phosphorylation of MAPKs and expressions of Sox9 and Co12A1 were observed by Western blotting or real-time PCR. Results Activation of RhoA brought about ROCK activation and Sox9 diminution. MAPKs were activated in LPA-treated cells, and inhibition of c-Jun terminal kinase (JNK) activity was sufficient for recovering Rho/ROCK-induced Sox9 diminution. Conclusion These data suggest a novel regulation mechanism that Rho/ROCK increases the phosphorylation of JNK and indirectly participates in the regulation of Sox9 transcription inchondrocytes. | |||||||||||||||||||||
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| 内容記述タイプ | Other | |||||||||||||||||||||
| 内容記述 | application/pdf | |||||||||||||||||||||