ID | 61093 |
フルテキストURL | |
著者 |
Nishida, Takashi
Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Kaken ID
publons
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Kubota, Satoshi
Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Kaken ID
publons
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抄録 | Cellular communication network factor 2 (CCN2) is a cysteine-rich secreted matricellular protein that regulates various cellular functions including cell differentiation. CCN2 is highly expressed under several types of mechanical stress, such as stretch, compression, and shear stress, in mesenchymal cells including chondrocytes, osteoblasts, and fibroblasts. In particular, CCN2 not only promotes cell proliferation and differentiation of various cells but also regulates the stability of mRNA of TRPV4, a mechanosensitive ion channel in chondrocytes. Of note, CCN2 behaves like a biomarker to sense suitable mechanical stress, because CCN2 expression is down-regulated when chondrocytes are subjected to excessive mechanical stress. These findings suggest that CCN2 is a mechano-sensing regulator. CCN2 expression is regulated by the activation of various mechano-sensing signaling pathways, e.g., mechanosensitive ion channels, integrin-focal adhesion-actin dynamics, Rho GTPase family members, Hippo-YAP signaling, and G protein-coupled receptors. This review summarizes the characterization of mechanoreceptors involved in CCN2 gene regulation and discusses the role of CCN2 as a mechano-sensing regulator of mesenchymal cell differentiation, with particular focus on chondrocytes.
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キーワード | Mechanoreceptors
Cellular communication network factor 2 (CCN2)
Mechanical stress
Chondrocytes
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発行日 | 2020-11
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出版物タイトル |
Japanese Dental Science Review
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巻 | 56巻
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号 | 1号
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出版者 | Elsevier
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開始ページ | 119
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終了ページ | 126
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ISSN | 1882-7616
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NCID | AA12334461
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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論文のバージョン | publisher
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PubMed ID | |
DOI | |
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関連URL | isVersionOf https://doi.org/10.1016/j.jdsr.2020.07.001
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ライセンス | http://creativecommons.org/licenses/by-nc-nd/4.0/
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助成機関名 |
日本学術振興会
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助成番号 | JP20K09889
JP19K22716
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