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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Circ_0002295 facilitated myocardial fibrosis progression through the miR-1287/CXCR2 axis
Guo-Bin Ma1, Wen-Xu Chen2, Fang-Jie Zhan2
1Department of Cardiology, Fuzhou Second Hospital, Fuzhou, China.
Abstract:
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.
Insights
Circular RNA circ_0002295 promotes myocardial fibrosis (MF) by regulating the miR-1287/CXCR2 axis. Targeting circ_0002295 offers a potential therapeutic strategy for treating MF.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- RNA Biology
Background:
- Myocardial fibrosis (MF) is a critical factor in cardiovascular diseases like hypertension and heart failure.
- Circular RNAs (circRNAs) have emerged as key regulators in the progression of MF.
Purpose of the Study:
- To investigate the role of circ_0002295 in myocardial fibrosis.
- To elucidate the regulatory mechanism involving circ_0002295, miR-1287, and CXCR2 in MF.
Main Methods:
- Quantification of circ_0002295, miR-1287, and CXCR2 levels in MF patients.
- Functional assays including knockdown of circ_0002295 and silencing of CXCR2.
- Molecular mechanism studies to determine interactions between circ_0002295, miR-1287, and CXCR2.
Main Results:
- Circ_0002295 and CXCR2 were upregulated, while miR-1287 was downregulated in MF patients.
- Knockdown of circ_0002295 inhibited proliferation, migration, and MF progression.
- Circ_0002295 acted as a molecular sponge for miR-1287, and miR-1287 targeted CXCR2, forming the circ_0002295/miR-1287/CXCR2 axis.
Conclusions:
- Circ_0002295 promotes MF progression by modulating the miR-1287/CXCR2 pathway.
- Circ_0002295 represents a potential therapeutic target for myocardial fibrosis.
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