Circ_0002295 facilitated myocardial fibrosis progression through the miR-1287/CXCR2 axis

被引:2
|
作者
Ma, Guo-Bin [1 ]
Chen, Wen-Xu [2 ]
Zhan, Fang-Jie [2 ]
Xie, Wen-Jing [2 ]
Chen, Rong-Wei [2 ]
Chen, Hong [2 ]
Ye, Wei-Lin [2 ]
Jiang, Yu [2 ]
Xu, Jian-Ping [3 ]
机构
[1] Fuzhou Second Hosp, Dept Cardiol, 47 Shang Teng Rd, Fuzhou 350007, Fujian, Peoples R China
[2] Fuzhou Second Hosp, Dept Clin Lab, 47 Shang Teng Rd, Fuzhou 350007, Fujian, Peoples R China
[3] Fujian Med Univ, Dept Clin Lab Med, 88 Jiao Tong Rd, Fuzhou 350004, Peoples R China
关键词
cardiac myofibroblasts; circ_0002295; CXCR2; miR-1287; myocardial fibrosis; CARDIAC FIBROSIS; CIRCULAR RNAS; CHEMOKINES; MICRORNAS;
D O I
10.1111/1440-1681.13819
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Myocardial fibrosis (MF) is involved in hypertension, myocardial infarction and heart failure. It has been reported that circular RNA (circRNA) is a key regulatory factor of MF progression. In this study, we revealed that circ_0002295 and CXCR2 were elevated, and miR-1287 was reduced in MF patients. Knockdown of circ_0002295 effectively suppressed the proliferation, migration and MF progression. Circ_0002295 was the molecular sponge of miR-12878, and miR-1287 inhibitor reversed the biological functions of circ_0002295 on the myocardial fibrosis. CXCR2 was a target gene of miR-1287, and CXCR2 silencing relieved the impacts of miR-1287 inhibitor on cardiac myofibroblasts. Circ_0002295 promoted MF progression by regulating the miR-1287/CXCR2 axis, providing a possible circRNA-targeted therapy for MF.
引用
收藏
页码:944 / 953
页数:10
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