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  1. Public
  2. 研究紀要
  3. ACTA MEDICA KINDAI UNIVERSITY
  4. 38(2)2013
  1. Private
  2. 研究紀要
  3. Acta medica Kinki University
  4. 38(2)2013

<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/10566
176f0bd9-48fd-4899-99da-167f415c3a9b
名前 / ファイル ライセンス アクション
AA0050842-20131200-0091.pdf AA0050842-20131200-0091.pdf (697.1 kB)
Item type ☆紀要論文 / Departmental Bulletin Paper(1)
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

Onodera, Yuta

ja-Kana オノデラ, ユウタ

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Teramura, Takeshi

× Teramura, Takeshi

Teramura, Takeshi

ja-Kana テラムラ, タケシ

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Takehara, Toshiyuki

× Takehara, Toshiyuki

Takehara, Toshiyuki

ja-Kana タケハラ, トシユキ

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Fukuda, Kanji

× Fukuda, Kanji

Fukuda, Kanji

ja-Kana フクダ, カンジ

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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
著者 所属
値 Institute of Advanced Clinical Medicine
著者 所属
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
著者所属(翻訳)
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
ISSN
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 application/pdf
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