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  1. 学術雑誌論文

Protective Role of Cardiac CFTR Activation Upon Early Reperfusion Against Myocardial Infarction

https://doi.org/10.57426/00000757
https://doi.org/10.57426/00000757
c525ef12-8606-426b-a983-dca78283cf7d
名前 / ファイル ライセンス アクション
CellPhysiolBiochem_v30_p1023-1038.pdf CellPhysiolBiochem_v30_p1023-1038.pdf (1.8 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2013-09-27
タイトル
タイトル Protective Role of Cardiac CFTR Activation Upon Early Reperfusion Against Myocardial Infarction
タイトル
タイトル Protective Role of Cardiac CFTR Activation Upon Early Reperfusion Against Myocardial Infarction
言語 en
言語
言語 eng
キーワード
言語 en
主題Scheme Other
主題 CFTR
キーワード
言語 en
主題Scheme Other
主題 Anion channel
キーワード
言語 en
主題Scheme Other
主題 Ischemia
キーワード
言語 en
主題Scheme Other
主題 Reperfusion
キーワード
言語 en
主題Scheme Other
主題 Myocardial infarction
キーワード
言語 en
主題Scheme Other
主題 Necrosis
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
ID登録
ID登録 10.57426/00000757
ID登録タイプ JaLC
著者 浦本, 裕美

× 浦本, 裕美

浦本, 裕美

ja-Kana ウラモト, ヒロミ

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Uramoto, Hiromi

× Uramoto, Hiromi

en Uramoto, Hiromi

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Okada, Toshiaki

× Okada, Toshiaki

en Okada, Toshiaki

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Okada, Yasunobu

× Okada, Yasunobu

en Okada, Yasunobu

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抄録
内容記述タイプ Abstract
内容記述 Background: The cardiac isoform of the cystic fibrosis transmembrane conductance regulator(CFTR) was shown to be activated by β-adrenergic or purinergic stimulation and involved in cell volume regulation after osmotic swelling. Also, cardiac CFTR was reported to be essential in the mechanism by which ischemic preconditioning protects against ischemia/reperfusion(I/R)-induced injury of the heart. Here, we explored the possibility that activation of cardiac CFTR can provide protection against I/R-induced myocardial infarction, even after ischemic attack. Methods: The hearts of wild-type mice were subjected to 30- or 40-min left coronary artery occlusion followed by 2-h or 2-day reperfusion in vivo, and myocardial infarction was examined under a variety of conditions. Neonetal rat ventricular myocytes in primary culture were subjected to hypoxia/reoxygenation in vitro, and necrotic cell death was examined. Results: The infarct size was much greater in CFTR knockout mice than in wild-type mice. Intravenous infusion of a number of putative CFTR activators upon reperfusion prominently reduced the size of myocardial infarction in wild-type but not CFTR-deficient mice. This protective effect was abolished by co-administration of a CFTR inhibitor. CFTR activators ameliorated, in a manner sensitive to a CFTR inhibitor, release of myocardial-specific creatine kinase isoenzyme to the serum in mice subjected to I/R in vivo. Necrotic death of cultured neonatal rat ventricular myocytes subjected to hypoxia/reoxygenation in vitro was ameliorated by CFTR activators or CFTR gene overexpression but aggravated by a CFTR inhibitor or CFTR gene silencing. Conclusion: It is concluded that activation of endogenous myocardial CFTR upon early reperfusion is involved in protection against necrotic myocardial injury induced by I/R in vivo and in vitro. Cardiac CFTR may serve as a target accessible even after ischemic attack for pharmacotherapeutic intervention in I/R-induced myocardial infarction.
書誌情報 Cellular Physiology and Biochemistry
en : Cellular Physiology and Biochemistry

巻 30, 号 4, p. 1023-1038, 発行日 2012
出版者
出版者 Karger
ISSN
収録物識別子タイプ ISSN
収録物識別子 10158987
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
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