| Mitofusin 2 Inhibits Angiotensin II-Induced Myocardial Hypertrophy. | |
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MedLine Citation:
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PMID: 21106870 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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OBJECTIVES: Myocardial hypertrophy is a common clinical finding leading to heart failure and sudden death. Mitofusin 2 (Mfn2), a hyperplasia suppressor protein, is downregulated in hypertrophic heart. This study examined the role of Mfn2 in myocardial hypertrophy and its potential signal pathway. Methods and RESULTS: In in vitro studies, neonatal cardiac myocytes were isolated and cultured. Incubation of cultured cardiomycytes with angiotensin II (Ang II) inhibited gene expression of Mfn2; induced cell hypertrophy and protein synthesis; and activated protein kinase Akt. Pretreatment of cells with AdMfn2-a replication-deficient adenoviral vector encoding rat Mfn2 gene-upregulated Mfn2 expression and subsequently attenuated Ang II-induced cell hypertrophy; protein synthesis; and Akt activation. In in vivo studies, direct gene delivery of AdMfn2 into myocardium decreased the infusion of Ang II-induced atrial natriuretic factor (ANF, a hypertrophic marker) expression and cardiomyocyte cross-sectional area. Consistently, upregulation of Mfn2 in myocardium decreased the thicknesses of anterior and posterior walls of left ventricle (LV) and the ratio of LV mass/body weight in Ang II-treated rats. Of note, AdGFP (control for AdMfn2) did not affect the effects of Ang II in vitro or in vivo. CONCLUSIONS: Upregulation of Mfn2 inhibits Ang II-induced myocardial hypertrophy. In this process, inhibition of Akt activation seems to play a significant role. These findings indicate Mfn2 is a critical protein in modulating myocyte hypertrophy. |
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Authors:
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Haiyi Yu; Yanhong Guo; Lin Mi; Xueying Wang; Lei Li; Wei Gao |
Publication Detail:
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Type: Journal Article Date: 2010-11-24 |
Journal Detail:
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Title: Journal of cardiovascular pharmacology and therapeutics Volume: 16 ISSN: 1940-4034 ISO Abbreviation: J. Cardiovasc. Pharmacol. Ther. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-05-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9602617 Medline TA: J Cardiovasc Pharmacol Ther Country: United States |
Other Details:
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Languages: eng Pagination: 205-11 Citation Subset: IM |
Affiliation:
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Department of Cardiology, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education, Beijing, PR China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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