| 张梦伟,赵忠帅,杨林,王明,杨雪飞,王倩.SNHG6靶向miR-101/TGFBR1促进AMI小鼠左心室心肌纤维化.[J].中南医学科学杂志.,2023,(5):640-644. |
| SNHG6靶向miR-101/TGFBR1促进AMI小鼠左心室心肌纤维化 |
| SNHG6 targets miR-101/TGFBR1 to promote left ventricular myocardial fibrosis in AMI mice |
| 投稿时间：2022-08-28 修订日期：2023-08-08 |
| DOI：10.15972/j.cnki.43-1509/r.2023.05.004 |
| 中文关键词: AMI lncRNA SNHG6 miR-101-3p TGFBR1 H9C2 心肌纤维化 [ |
| 英文关键词:AMI lncRNA SNHG6 miR-101-3p TGFBR1 H9C2 myocardial fibrosis |
| 基金项目:山东省医药卫生发展计划项目(20203011333) |
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| 中文摘要: |
| 目的探讨SNHG6对急性心肌梗死(AMI)小鼠左心室心肌的影响。 方法将30只雄性C57/BL6小鼠构建成AMI小鼠后随机均分为AMI组、AMI+SNHG6组、AMI+miR-101-3p组、AMI+SNHG6+miR-101-3p组、AMI+miR-101-3p+TGFBR1组,另设正常小鼠6只为假手术组。qRT-PCR检测AMI小鼠SNHG6、miR-101-3p表达水平。心脏彩超检测各组小鼠左室射血分数(LVEF)；马松和天狼星红染色法以及免疫组化分析各组小鼠左心室心肌纤维化变化。将H9C2细胞株分为阴性对照组(转染空质粒)、SNHG6组(转染质粒SNHG6)、miR-101-3p组(转染质粒miR-101-3p)。Western blotting检测各组TGFBR1蛋白表达；采用双荧光素酶报告基因法预测并验证SNHG6/miR-101-3p/TGFBR1荧光素酶活性及调控机制。 结果AMI小鼠较假手术组SNHG6表达显著增加,miR-101-3p降低(P＜0.05)。与AMI组比较,AMI+SNHG6组小鼠LVEF降低,心肌纤维化程度加重(P＜0.05)；AMI+miR-101-3p组LVEF升高,心肌纤维化程度减轻(P＜0.05)。AMI+SNHG6+miR-101-3p组较AMI+SNHG6组LVEF升高、心肌纤维化程度减轻(P＜0.05),而AMI+miR-101-3p+TGFBR1组较AMI+miR-101-3p组LVEF降低、心肌纤维化程度加重(P＜0.05)。双荧光素酶报告基因法验证显示,miR-101-3p组SNHG6、TGFBR1野生型质粒的荧光素酶活性较阴性对照组明显降低(P＜0.05)。 结论SNHG6抑制miR-101-3p上调TGFBR1加重AMI小鼠左心室心肌纤维化。 |
| 英文摘要: |
| AimTo investigate the effects of the SNHG6 on the left ventricular myocardium in acute myocardial infarction (AMI) mice. MethodsTo establish a mouse model of AMI, male C57/BL6 mice (n＝30) were randomly divided into five groups:AMI group, AMI+SNHG6 group, AMI+miR-101-3p group, AMI+SNHG6+miR-101-3p group, AMI+miR-101-3p+TGFBR1 group, and another six normal mice were used as the sham-operation group. The expression levels of SNHG6 and miR-101-3p in AMI mice were detected by qRT-PCR. Left ventricular ejection fraction (LVEF) was detected by cardiac color Doppler ultrasound. Masson and Sirius red staining and immunohistochemistry were used to analyze the changes of left ventricular myocardial fibrosis in each group. The H9C2 cell line was divided into three groups:negative control group (transfected with empty plasmid), SNHG6 group (transfected with plasmid SNHG6), miR-101-3p group (transfected with plasmid miR-101-3p). Western blotting was used to detect TGFBR1 protein expression.The fluorescence reporter gene method was used to predict and verify the fluorescence activity and regulatory mechanism of SNHG6/miR-101-3p/TGFBR1. ResultsCompared with the sham-operation group, the expression of SNHG6 was significantly increased, while miR-101-3p was decreased in AMI mice (P＜0.05). Compared with the AMI group, the LVEF of mice in the AMI+SNHG6 group was reduced, and the degree of myocardial fibrosis aggravated (P＜0.05); the LVEF of mice in the AMI+miR-101-3p group was increased, and the degree of myocardial fibrosis was alleviated (P＜0.05). Compared with the AMI+SNHG6 group, the LVEF of mice in the AMI+SNHG6+miR-101-3p group was increased, and the degree of myocardial fibrosis was alleviated (P＜0.05). However, compared with the AMI+miR-101-3p group, the LVEF of mice in the AMI+miR-101-3p+TGFBR1 group was decreased, and the degree of myocardial fibrosis was aggravated (P＜0.05). The fluorescence reporter gene method showed that the luciferase activity of SNHG6 and TGFBR1 wild-type plasmids in the miR-101-3p group was significantly lower than that in the negative control group (P＜0.05). ConclusionSNHG6 inhibits miR-101-3p to upregulate TGFBR1 and aggravate left ventricular myocardial fibrosis in AMI mice. |
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