Xiao Yimin, Zhang Xiaofei, Fan Shihao, Cui Guanghao, Shen Zhenya
Department of Cardiovascular Surgery of the First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, China.
Department of Cardiovascular Surgery, Shanghai Yodak Cardiothracic Hospital, Shanghai, China.
PLoS One. 2016 Dec 16;11(12):e0168078. doi: 10.1371/journal.pone.0168078. eCollection 2016.
Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to overload pressure of heart. From abundant studies, a conclusion is drawn that many microRNAs (miRNAs) are associated with cardiac hypertrophy and heart failure. To investigate the role of microRNA-497 (miR-497) in myocardial hypertrophy, two models were established in this study from cell level to integral level. Cardiac hypertrophy was induced by using angiotensin Ⅱ (Ang Ⅱ) in vitro and was created by transverse abdominal aortic constriction (TAC) in vivo. There was a significant decrease expression of miR-497 in cardiac hypertrophy models. Moreover, overexpression of miR-497 inhibited myocardial hypertrophy both in vitro and in vivo without heart function variation. In addition, luciferase reporter assays demonstrated that Sirt4 was a direct target gene of miR-497. Taking together, our study indicates that miR-497 modulates cardiac hypertrophy by targeting Sirt4 and may serve as a potential therapeutic substance in the course.
心肌肥大是心肌对心脏压力过载的一种适应性增大。大量研究得出结论，许多微小RNA（miRNA）与心肌肥大和心力衰竭有关。为了研究微小RNA - 497（miR - 497）在心肌肥大中的作用，本研究从细胞水平到整体水平建立了两种模型。体外使用血管紧张素Ⅱ（AngⅡ）诱导心肌肥大，体内通过腹主动脉缩窄（TAC）造成心肌肥大。在心肌肥大模型中，miR - 497的表达显著降低。此外，miR - 497的过表达在体外和体内均抑制心肌肥大，且不影响心脏功能。另外，荧光素酶报告基因检测表明Sirt4是miR - 497的直接靶基因。综上所述，我们的研究表明miR - 497通过靶向Sirt4调节心肌肥大，可能是该过程中的一种潜在治疗物质。
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