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首页> 外文期刊>Journal of Cellular Physiology >MiR-133a regulates collagen 1A1: potential role of miR-133a in myocardial fibrosis in angiotensin II-dependent hypertension.
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MiR-133a regulates collagen 1A1: potential role of miR-133a in myocardial fibrosis in angiotensin II-dependent hypertension.

机译：mir - 133 - 1调节胶原蛋白a1:潜在的作用mir - 133——在心肌纤维化血管紧张素II-dependent高血压。

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摘要

MicroRNAs play an important role in myocardial diseases. MiR-133a regulates cardiac hypertrophy, while miR-29b is involved in cardiac fibrosis. The aim of this study was to evaluate whether miR-133a and miR-29b play a role in myocardial fibrosis caused by Angiotensin II (Ang II)-dependent hypertension. Sprague-Dawley rats were treated for 4 weeks with Ang II (200 ng/kg/min) or Ang II + irbesartan (50 mg/kg/day in drinking water), or saline by osmotic minipumps. At the end of the experimental period, cardiac miR-133a and miR-29b expression was measured by real-time PCR, and myocardial fibrosis was evaluated by morphometric analysis. A computer-based prediction algorithm led to the identification of collagen 1a1 (Col1A1) as a putative target of miR-133a. A reporter plasmid bearing the 3'-untranslated regions (UTRs) of Col1A1 mRNA was constructed and luciferase assay was performed. MiR-133a suppressed the activity of luciferase when the reporter gene was linked to a 3'-UTR segment of Col1A1 (P < 0.01). Mutation of miR-133a binding sites in the 3'-UTR of Col1A1 mRNA abolished miR-133a-mediated repression of reporter gene activity, showing that Col1A1 is a real target of miR-133a. In vivo, Ang II caused an increase in systolic blood pressure (P < 0.0001, tail cuff) and myocardial fibrosis in presence of a decrease in miR-133a (P < 0.01) and miR-29b (P < 0.01), and an increase in Col1A1 expression (P < 0.01). These effects were abolished by Ang II administration + irbesartan. These data demonstrate a relationship between miR-133a and Col1A1, suggesting that myocardial fibrosis occurring in Ang II-dependent hypertension is regulated by the down-regulation of miR-133a and miR-29b through the modulation of Col1A1 expression.
机译：小分子核糖核酸心肌中发挥重要作用疾病。虽然miR-29b参与心脏纤维化。本研究的目的是评估是否mir - 133 a和miR-29b在心肌中发挥作用纤维化引起的血管紧张素ⅱ(Ang2)端依赖高血压。治疗4周,Ang II (200通过渗透饮用水中)或生理盐水微型泵。心脏mir - 133 a和miR-29b表达以实时PCR和心肌纤维化是由地貌形态示量评估分析。导致了一个基于计算机的预测算法胶原蛋白的识别1 a1 (Col1A1)mir - 133 a的假定的目标。轴承的3 '非翻译区(utr)Col1A1 mRNA构造和荧光素酶检测是执行。的荧光素酶报告基因时联系3’utr段Col1A1 (P < 0.01)。突变mir - 133 - 3’utr结合位点Col1A1 mRNA废除mir - 133 - a -介导的报告基因的镇压活动,展示Col1A1是mir - 133 a的真正目标。体内,Angⅱ收缩压的增加引起的压力(P < 0.0001,尾袖)和心肌纤维化的存在降低mir - 133 a (P< 0.01)和miR-29b (P < 0.01),增加在Col1A1表达(P < 0.01)。废除了Angⅱ管理+irbesartan。mir - 133 - a和Col1A1,暗示心肌纤维化发生在盎II-dependent高血压是由下调mir - 133 a和miR-29b通过调制Col1A1表达式。

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