Abstract
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 up-regulation of miR-132 improved the cardiac dysfunction, attenuated cardiac fibrosis in heart failure via inhibiting PTEN expression, and attenuating PI3K/Akt signal pathway. Up-regulation of miR-132 may be a strategy for the treatment of heart failure and cardiac fibrosis.
Highlights
Heart failure, a complex syndrome resulting from structural or functional cardiac disorders, can disable the ventricle from ejecting or filling blood [1,2,3]
Heart failure is preceded by left ventricular (LV) remodeling, which is characterized by the formation of cardiac interstitial fibrosis, including the increases of collagen I, collagen III, α-smooth muscle actin (α-SMA), and transforming growth factor-β (TGF-β) [7,8,9]
We found that attenuated cardiac function in myocardial infarction (MI)-induced heart failure rats, which was improved by miR-132 agomiR but aggravated by miR-132 antagomiR treatment
Summary
A complex syndrome resulting from structural or functional cardiac disorders, can disable the ventricle from ejecting or filling blood [1,2,3]. Despite the progress in diagnosis, heart failure is still a leading cause of morbidity and mortality worldwide [4,5,6]. Heart failure is preceded by left ventricular (LV) remodeling, which is characterized by the formation of cardiac interstitial fibrosis, including the increases of collagen I, collagen III, α-smooth muscle actin (α-SMA), and transforming growth factor-β (TGF-β) [7,8,9]. Human studies and animal experiments have found multiple miRs, including miR-24, -199b, -100, -195, -208, and -133, are dysregulated in heart failure [15,16,17,18,19].
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