Feng Gao, Yan Zhang, Li Chuanchuan, Hou Yuemei
The Third Clinical Medical College of Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Fuzhou First Hospital Affiliated to Fujian Medical University, Fuzhou, Fujian 350000, P.R. China.
Mol Med Rep. 2016 Aug;14(2):1631-5. doi: 10.3892/mmr.2016.5402. Epub 2016 Jun 14.
The expression level of microRNA-208a (miR-208a) in a rat model with myocardial infarction and the effect of cAMP-PKA signaling pathway in early stage of myocardial infarction in rats were investigated. The early myocardial infarction model was established in 12 male Sprague-Dawley rats by ligation of the anterior descending coronary artery, and 12 rats were selected as the control group (sham operation group). Reverse-transcription quantitative PCR was conducted to detect the expression levels of miR-208a in the myocardium of and the expression levels of miR‑208a in the serum of rats in the two groups. Western blot analysis was used to evaluate the expression levels of cAMP-PKA protein in the rat tissues in the two groups. After stimulating high levels of miR‑208a expression in human myocardial cells (HCM), western blot analysis was used to detect the cAMP-PKA protein levels. The expression levels of miR‑208a in myocardial tissues in rats with myocardial infarction were significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The expression levels of miR‑208a in the early stage of myocardial infarction rats were also significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The level of cAMP-PKA protein in myocardial tissue in rats with chronic myocardial infarction was also significantly higher. Transfection of human myocardial cells with miR‑208a analogue significantly increased the cAMP-PKA protein levels in human myocardial cells. In conclusion, the over-expression of miR-208a in myocardial infarction tissue and the high levels of this miRNA in the serum, may be involved in the process of myocardial infarction by influencing the cAMP-PKA signaling pathway in myocardial cells.
研究了微小RNA-208a（miR-208a）在大鼠心肌梗死模型中的表达水平以及cAMP-PKA信号通路在大鼠心肌梗死早期的作用。通过结扎冠状动脉前降支，在12只雄性Sprague-Dawley大鼠中建立早期心肌梗死模型，选取12只大鼠作为对照组（假手术组）。采用逆转录定量PCR检测两组大鼠心肌组织中miR-208a的表达水平以及血清中miR-208a的表达水平。采用蛋白质免疫印迹分析评估两组大鼠组织中cAMP-PKA蛋白的表达水平。在人心肌细胞（HCM）中刺激miR-208a高水平表达后，采用蛋白质免疫印迹分析检测cAMP-PKA蛋白水平。心肌梗死大鼠心肌组织中miR-208a的表达水平显著高于对照组，差异具有统计学意义（P<0.05）。心肌梗死早期大鼠miR-208a的表达水平也显著高于对照组，差异具有统计学意义（P<0.05）。慢性心肌梗死大鼠心肌组织中cAMP-PKA蛋白水平也显著升高。用miR-208a类似物转染人心肌细胞可显著提高人心肌细胞中cAMP-PKA蛋白水平。综上所述，miR-208a在心肌梗死组织中的过表达以及血清中该微小RNA的高水平，可能通过影响心肌细胞中的cAMP-PKA信号通路参与心肌梗死过程。
