有氧运动对心肌梗死后大鼠心肌间质胶原生成中 miR-29a 和 miR-101a 表达的影响。
Effects of miR-29a and miR-101a Expression on Myocardial Interstitial Collagen Generation After Aerobic Exercise in Myocardial-infarcted Rats.
机构信息
Co-Innovation Center for Qinba Region Sustainable Development, Institute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an, Shaanxi, China.
The High School Affiliated to Shaanxi Normal University, Xi'an, Shaanxi, China.
出版信息
Arch Med Res. 2017 Jan;48(1):27-34. doi: 10.1016/j.arcmed.2017.01.006.
BACKGROUND AND AIMS
Myocardial infarction (MI) is accompanied by increased collagen deposition, cell necrosis and angiogenesis in cardiac tissue, which results in reduced ventricular compliance. Both microRNA-29a (miR-29a) and microRNA-101a (miR-101a) target the mRNAs encoding collagens and other proteins involved in fibrosis.
METHODS
We assessed the effects of intermittent aerobic exercise on the expression of cardiac miR-29a and miR-101a and following effects on the TGFβ, fos, Smad2/3, COL1A1 and COL3A1 in MI model of rats. Intermittent aerobic exercise for MI rats was begun from the second week and ended at the ninth week postsurgery. Expressions of microRNAs (miRNAs) and fibrosis-associated genes were detected from the infarction adjacent region located in the left ventricle. The heart coefficient (HC = heart weight/body weight) and hemodynamics assay were used to evaluate cardiac function level.
RESULTS
Intermittent aerobic exercise inhibited myocardial interstitial collagen deposition and significantly improved cardiac function of MI rats. The results of real-time PCR and Western blot indicate that intermittent aerobic exercise enhanced the expression of miR-29a and miR-101a and inhibited TGFβ pathway in the MI rats.
CONCLUSIONS
Our results suggest that controlled intermittent aerobic exercise can inhibit TGFβ pathway via up-regulation to the expression of miR-29a and miR-101a and finally cause a reduced fibrosis and scar formation in cardiac tissue. We believe that controlled intermittent aerobic exercise is beneficial to the healing and discovery of damaged cardiac tissues and their function after MI.
背景与目的
心肌梗死（MI）伴随着心肌组织中胶原蛋白沉积、细胞坏死和血管生成增加，导致心室顺应性降低。miR-29a 和 miR-101a 均可靶向编码胶原和其他纤维化相关蛋白的 mRNA。
方法
我们评估了间歇有氧运动对 MI 大鼠心脏 miR-29a 和 miR-101a 表达的影响，以及对 TGFβ、fos、Smad2/3、COL1A1 和 COL3A1 的后续影响。MI 大鼠的间歇有氧运动从术后第二周开始，第九周结束。从左心室梗死相邻区域检测 miRNA（miRNAs）和纤维化相关基因的表达。心脏系数（HC=心脏重量/体重）和血液动力学检测用于评估心脏功能水平。
结果
间歇有氧运动抑制了心肌间质胶原沉积，显著改善了 MI 大鼠的心脏功能。实时 PCR 和 Western blot 结果表明，间歇有氧运动增强了 MI 大鼠 miR-29a 和 miR-101a 的表达，并抑制了 TGFβ 通路。
结论
我们的结果表明，受控间歇有氧运动可通过上调 miR-29a 和 miR-101a 的表达来抑制 TGFβ 通路，最终导致心肌组织中纤维化和瘢痕形成减少。我们认为，受控间歇有氧运动有利于 MI 后受损心脏组织的愈合和发现及其功能的恢复。
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