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Protective effects of intercalated disk protein afadin on chronic pressure overload-induced myocardial damage.
http://hdl.handle.net/10422/12233
http://hdl.handle.net/10422/12233be4d2f23-6753-457f-925a-0e315be3fded
名前 / ファイル | ライセンス | アクション |
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srep39335.pdf (4.1 MB)
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This work is licensed under a Creative Commons Attribution 4.0 International License. The images
or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-01-11 | |||||
タイトル | ||||||
タイトル | Protective effects of intercalated disk protein afadin on chronic pressure overload-induced myocardial damage. | |||||
言語 | ||||||
言語 | eng | |||||
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 | journal article | |||||
著者 |
ZANKOV, Dimitar Petrov
× ZANKOV, Dimitar Petrov× SHIMIZU, Akio× TANAKA-OKAMOTO, Miki× MIYOSHI, Jun× 扇田, 久和 |
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著者別名 |
清水, 昭男
× 清水, 昭男× 扇田, 久和 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Adhesive intercellular connections at cardiomyocyte intercalated disks (IDs) support contractile force and maintain structural integrity of the heart muscle. Disturbances of the proteins at IDs deteriorate cardiac function and morphology. An adaptor protein afadin, one of the components of adherens junctions, is expressed ubiquitously including IDs. At present, the precise role of afadin in cardiac physiology or disease is unknown. To explore this, we generated conditional knockout (cKO) mice with cardiomyocyte-targeted deletion of afadin. Afadin cKO mice were born according to the expected Mendelian ratio and have no detectable changes in cardiac phenotype. On the other hand, chronic pressure overload induced by transverse aortic constriction (TAC) caused systolic dysfunction, enhanced fibrogenesis and apoptosis in afadin cKO mice. Afadin deletion increased macrophage infiltration and monocyte chemoattractant protein-1 expression, and suppressed transforming growth factor (TGF) β receptor signaling early after TAC procedure. Afadin also associated with TGFβ receptor I at IDs. Pharmacological antagonist of TGFβ receptor I (SB431542) augmented mononuclear infiltration and fibrosis in the hearts of TAC-operated control mice. In conclusion, afadin is a critical molecule for cardiac protection against chronic pressure overload. The beneficial effects are likely to be a result from modulation of TGFβ receptor signaling pathways by afadin. | |||||
書誌情報 |
Scientific Reports 巻 7, p. 39335, 発行日 2017-01-03 |
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出版者 | ||||||
出版者 | Nature Publishing Group | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 2045-2322 | |||||
PMID | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | PMID | |||||
関連識別子 | 28045017 | |||||
PMCID | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.ncbi.nlm.nih.gov/pmc/articles/pmc5206728/ | |||||
関連名称 | PMC5206728 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1038/srep39335 | |||||
関連名称 | 10.1038/srep39335 | |||||
権利 | ||||||
権利情報 | © The Author(s) 2017 | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | ||||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
資源タイプ | ||||||
内容記述タイプ | Other | |||||
内容記述 | Journal Article |