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  • Title: [Overexpression of miR-130a-3p attenuates cardiomyocyte hypertrophy].
    Author: Wang X, Qu J, Li D, Li J, Wu W, Liu X.
    Journal: Sheng Wu Yi Xue Gong Cheng Xue Za Zhi; 2020 Apr 25; 37(2):340-348. PubMed ID: 32329288.
    Abstract:
    This study aimed to explore the role of miR-130a-3p in cardiomyocyte hypertrophy and its underlying mechanisms. Pressure-overload induced myocardial hypertrophy mice model was constructed by thoracic aortic constriction (TAC). In vitro, norepinephrine (NE) was used to stimulate neonatal rat cardiomyocytes (NRCMs) and H9c2 rat cardiomyocytes to induce hypertrophic phenotypes. The expression of miR-130a-3p was detected in mice hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. The mimics and inhibitors of miR-130a-3p were transfected into H9c2 cells to observe the role of miR-130a-3p on the hypertrophic phenotype change of cardiomyocytes separately. Furthermore, whether miR-130a-3p regulated hypertrophic related signaling pathways was explored. The results showed that the expression of miR-130a-3p was significantly decreased in hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. After transfection of miR-130a-3p mimics, the expression of hypertrophic marker genes, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), and the cell surface area were notably down-regulated compared with the control group (mimics N.C. + NE group). But after transfection of miR-130a-3p inhibitor, the expression of ANP, BNP and β-MHC in H9c2 cells increased significantly, and the cell area increased further. By Western blot, it was found that the protein phosphorylation level of Akt and mTOR were down-regulated after over-expression of miR-130a-3p. These results suggest that miR-130a-3p mimics may alleviate the degree of cardiomyocyte hypertrophy, meanwhile its inhibitor can further aggravate cardiomyocyte hypertrophy. Over-expression of miR-130a-3p may attenuate cardiomyocytes hypertrophy by affecting the Akt pathway. 本研究旨在探索 miR-130a-3p 对心肌细胞肥大的作用及其可能机制。通过胸主动脉缩窄法（TAC）构建压力超负荷所致心肌肥厚小鼠模型。使用去甲肾上腺素（NE）刺激 SD 乳鼠原代心肌细胞（NRCMs）及 H9c2 大鼠心肌细胞系，诱导这两种心肌细胞发生肥大表型转变。检测 miR-130a-3p 的表达变化，并进一步探索其对心肌细胞肥大是否有调控作用。结果表明，miR-130a-3p 在肥厚心肌组织、肥大 NRCMs 及 H9c2 细胞中的表达均明显降低。给予 miR-130a-3p mimics 使其过表达后，H9c2 细胞中肥大标志基因心房利钠肽（ANP）、脑利钠肽（BNP）和肌球蛋白重链 β（β-MHC）的表达较对照组（mimics N.C.+NE 组）明显下调，且细胞面积明显减小。而给予 miR-130a-3p inhibitor 抑制其表达后，肥大心肌细胞中 ANP、BNP、β-MHC 的表达进一步上升，且细胞面积进一步增加。Western blot 检测发现，过表达 miR-130a-3p 后心肌细胞中磷酸化 Akt 和磷酸化 mTOR 的表达水平下调。以上结果提示，miR-130a-3p mimics 可缓解心肌细胞肥大的程度；其 inhibitor 则可使心肌细胞肥大进一步加剧。过表达 miR-130a-3p 可能通过影响 Akt 通路来缓解 H9c2 心肌细胞肥大的程度。.
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