The aim of the present study was to determine the effect of microRNA (miR)-132 on cardiac fibrosis in myocardial infarction (MI)-induced heart failure and angiotensin (Ang) II-treated cardiac fibroblasts (CFs). Experiments were carried out in Sprague-Dawley rat treatment with ligation of left coronary artery to induce heart failure, and in CFs administration of Ang II to induce fibrosis. The level of miR-132 was increased in the heart of rats with MI-induced heart failure and the Ang II-treated CFs. In MI rats, left ventricle (LV) ejection fraction, fractional shortening, the maximum of the first differentiation of LV pressure (LV +dp/dtmax) and decline (LV -dp/dtmax) and LV systolic pressure (LVSP) were reduced, and LV end-systolic diameter (LVESD), LV end-diastolic diameter (LVEDD), LV volumes in systole (LVVS) and LV volumes in diastole (LVVD) were increased, which were reversed by miR-132 agomiR but deteriorated by miR-132 antagomiR. The expression levels of collagen I, collagen III, transforming growth factor-β (TGF-β), and α-smooth muscle actin (α-SMA) were increased in the heart of rat with MI-induced heart failure and CFs administration of Ang II. These increases were inhibited by miR-132 agomiR but enhanced by miR-132 antagomiR treatment. MiR-132 inhibited PTEN expression, and attenuated PI3K/Akt signal pathway in CFs. These results indicated that the upregulation of miR-132 improved the cardiac dysfunction, attenuated cardiac fibrosis in heart failure via inhibiting PTEN expression, and attenuating PI3K/Akt signal pathway. Upregulation of miR-132 may be a strategy for the treatment of heart failure and cardiac fibrosis.

中文翻译：

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MicroRNA-132减轻了心肌梗塞诱发的心力衰竭大鼠的心脏纤维化。

本研究的目的是确定microRNA（miR）-132对心肌梗死（MI）诱发的心力衰竭和血管紧张素（Ang）II治疗的心脏成纤维细胞（CFs）心脏纤维化的影响。实验是在结扎左冠状动脉以诱发心力衰竭的Sprague-Dawley大鼠治疗中，以及在CFs给予Ang II诱导纤维化中进行的。在MI诱发的心力衰竭和Ang II治疗的CF的大鼠心脏中，miR-132的水平升高。在MI大鼠中，左心室（LV）射血分数，分数缩短，LV压力（LV + dp / dtmax）和下降（LV -dp / dtmax）和LV收缩压（LVSP）的第一次分化最大值均降低，和左室舒张末期直径（LVESD），左室舒张末期直径（LVEDD），收缩期（LVVS）的左室容积和舒张期（LVVD）的左室容积增加，被miR-132 agomiR逆转，但被miR-132 antagomiR恶化。MI诱发的心力衰竭和CFs给予Ang后，大鼠心脏中的I型胶原，III型胶原，转化生长因子-β（TGF-β）和α-平滑肌肌动蛋白（α-SMA）的表达水平升高。二。这些增加被miR-132 agomiR抑制，但被miR-132 antagomiR治疗增强。MiR-132抑制CFs中PTEN的表达，并减弱PI3K / Akt信号通路。这些结果表明，miR-132的上调通过抑制PTEN表达和减弱PI3K / Akt信号通路，改善了心脏功能障碍，减轻了心力衰竭中的心脏纤维化。