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MiR-30e Attenuates Isoproterenol-induced Cardiac Fibrosis Through Suppressing Snail/TGF-beta Signaling 期刊论文

编号：

9aa0dd7d-faa5-4990-92d6-19ab4eca779a
作者：

Zhang, Wenqi(张文琪)#^[1]Chang, Hong(常宏)^[1]Zhang, Hexun^[2];Zhang, Lei(张蕾)*^[1]
语种：

英文
期刊：

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY ISSN：0160-2446 2017 年 70 卷 6 期 (362 - 368) ; DEC
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关键词：

miR-30e cardiac fibrosis Snail
摘要：

Background: MicroRNAs are a class of small RNA molecules that inhibit protein expression through either degradation of messenger RNA or interference with protein translation. Our previous work suggested an involvement of miR-30e in myocardial fibrosis; however, the exact role of miR-30e in the pathogenesis of cardiac fibrosis and the underlying mechanisms are not known.
Methods: Male Sprague Dawley rats were treated with isoproterenol (ISO) to induce cardiac remodeling and fibrosis and treated with either miR-30e agomir (AG) or antagomir and respective controls. The expression of miR-30e was evaluated by reverse transcription and quantitative polymerase chain reaction. Myocardial fibrosis was assessed by Masson's trichrome staining, and the level of oxidative stress and the expression of Snail and transforming growth factorbeta (TGF-b) were detected using Western blots.
Results: A significant downregulation of miR-30e was found in the hearts of ISO-treated rats with cardiac fibrosis compared with nontreated controls. In vivo administration of miR-30e AG increased the survival of ISO-treated rats compared with AG-negative control administration, which was associated with reduced oxidative stress. We further identified Snail as a novel miR-30e target. Snail expression was significantly increased in hearts from ISO-treated rats, which coincided with decreased miR-30e expression and increased TGF-b expression. An miR-30e putative target sequence was identified in the 30-untranslated wregion (UTR) Snail. In a reporter assay, miR-30e greatly suppressed the activity of wild-type 30-UTR-fused luciferase reporter, but showed no significant effect with the mutated 30UTR-fused reporter.
Conclusion: MiR-30e attenuated ISO-induced cardiac dysfunction and cardiac fibrosis in a rat cardiac remodeling model. Mechanistically, miR-30e suppressed Snail/TGF-beta pathway which was involved in ISO-induced cardiac remodeling.
推荐引用方式
GB/T 7714：

Zhang Wenqi,Chang Hong,Zhang Hexun, et al. MiR-30e Attenuates Isoproterenol-induced Cardiac Fibrosis Through Suppressing Snail/TGF-beta Signaling [J].JOURNAL OF CARDIOVASCULAR PHARMACOLOGY,2017,70(6):362-368.
APA：

Zhang Wenqi,Chang Hong,Zhang Hexun,Zhang Lei.(2017).MiR-30e Attenuates Isoproterenol-induced Cardiac Fibrosis Through Suppressing Snail/TGF-beta Signaling .JOURNAL OF CARDIOVASCULAR PHARMACOLOGY,70(6):362-368.
MLA：

Zhang Wenqi, et al. "MiR-30e Attenuates Isoproterenol-induced Cardiac Fibrosis Through Suppressing Snail/TGF-beta Signaling" .JOURNAL OF CARDIOVASCULAR PHARMACOLOGY 70,6(2017):362-368.
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