MicroR-26b Targets High Mobility Group, AT-hook 2 to Ameliorate Myocardial Infarction-induced Fibrosis by Suppression of Cardiac Fibroblasts Activation
MicroR-26b Targets High Mobility Group, AT-hook 2 to Ameliorate Myocardial Infarction-induced Fibrosis by Suppression of Cardiac Fibroblasts Activation
复制标题
DOI：
10.2174/1567202617666200506101258
复制
发表时间：
2020-01-01
影响因子：
2.1
通讯作者：
Deng, Xuejun
中科院分区：
文献类型：
--
作者：
Chen, Xiao;Ding, Zhaosheng;Deng, Xuejun
背景：心肌纤维化（myocardial Fibrosis，MF）是心肌梗死（myocardial infarction，MI）后的一种重要生理变化. MicroRNA-26 b（MiR-26 b）对肺纤维化有一定的抑制作用。方法：40只雄性SD大鼠随机分为4组（n=10）：假手术组（Sham）、MF组、MF +阴性对照（NC）阿戈米尔组（agomir）和MF + miR-26 b阿戈米尔组（agomir + miR-26 b）。从心脏组织中分离心脏成纤维细胞。采用MASSON染色检测纤维化程度，RT-qPCR、Western blotting和免疫组化检测纤维化相关基因的表达。利用TargetScan和双荧光素酶报告基因分析来预测miR-26 b与高迁移率基团AT-hook 2（HMGA 2）的关系。结果：研究发现MF大鼠心肌中miR-26 b的表达下调（P
Background: Myocardial Fibrosis (MF) is an important physiological change after myocardial infarction (MI). MicroRNA-26b (MiR-26b) has a certain inhibitory effect on pulmonary fibrosis. However, the role of miR-26b in MI-induced MF rats and underlying molecular mechanisms remain unknown.Methods: Forty male Sprague Dawley (SD) rats weighing 200-250 g were divided into four groups (n=10): Sham group, MF group, MF + negative control (NC) agomir group and MF + miR-26b agomir group. Cardiac fibroblasts were isolated from cardiac tissue. Fibrosis levels were detected by MASSON staining, while the expression of related genes was detected by RT-qPCR, Western blotting and Immunohistochemistry, respectively. TargetScan and dual-luciferase reporter assay were utilized to predict the relationship between miR-26b and high mobility group, AT-hook 2 (HMGA2).Results: The study found the expression of miR-26b to be down-regulated in the myocardium of MF rats (P