miR‐19b controls cardiac fibroblast proliferation and migration

Abstract

Cardiac fibrosis is a fundamental constituent of a variety of cardiac dysfunction, making it a leading cause of death worldwide. However, no effective treatment for cardiac fibrosis is available. Therefore, novel therapeutics for cardiac fibrosis are highly needed. Recently, miR‐19b has been found to be able to protect hydrogen peroxide (H2O2)‐induced apoptosis and improve cell survival in H9C2 cardiomyocytes, while down‐regulation of miR‐19b had opposite effects, indicating that increasing miR‐19b may be a new therapeutic strategy for attenuating cellular apoptosis during myocardial ischaemia–reperfusion injury. However, considering the fact that microRNAs might exert a cell‐specific role, it is highly interesting to determine the role of miR‐19b in cardiac fibroblasts. Here, we found that miR‐19b was able to promote cardiac fibroblast proliferation and migration. However, miR‐19b mimics and inhibitors did not modulate the expression level of collagen I. Pten was identified as a target gene of miR‐19b, which was responsible for the effect of miR‐19b in controlling cardiac fibroblast proliferation and migration. Our data suggest that the role of miR‐19b is cell specific, and systemic miR‐19b targeting in cardiac remodelling might be problematic. Therefore, it is highly needed and also urgent to investigate the role of miR‐19b in cardiac remodelling in vivo.

Long non‐coding RNA cardiac hypertrophy‐associated regulator governs cardiac hypertrophy via regulating miR‐20b and the downstream PTEN/AKT pathway

“…According to previous report, up-regulation of miR-19b inhibits apoptosis and activates the AKT pathway by down-regulating PTEN. 52 Here, we performed bioinformatics analysis using the RegRNA 2.0 database (http://regrna.mbc.nctu.edu.tw/html/predi ction.html) to identify the miRNAs that contain potential binding sequences for CHAR. The database predicts no potential binding site or sequence complementarity between CHAR and miR-19b.…”

Diagnostic value of circulating microRNA‐19b in heart failure

“…Over-expression of miR-19b decreased the infarct area and restored the left ventricular systolic function and volume load of mice with HF after myocardial infarction (MI) by inhibiting cardiac apoptosis. 10,11 According to a recent review, an important factor driving progression from myocardial hypertrophy to HFpEF was the proliferation of an abnormal fibroblast phenotype, which may degrade normal stromal matrix and was replaced by a fibrotic matrix structure. 12 Ravassa et al 13 reported that HFpEF was characterized by increased collagen cross-linking and involved in left ventricular diastolic dysfunction.…”

Integrative analysis of competing endogenous RNA networks reveals the functional lncRNAs in heart failure

“…Mir‐148 was a repressor of NF‐kB signalling, playing roles in cardiac injury 32. In addition, miR‐19 was demonstrated to involve in cardiac remodelling by controlling cardiac fibroblast proliferation and migration 33. Moreover, in “loss” module, a number of heart failure‐related miRNAs were also extracted.…”

“…32 In addition, miR-19 was demonstrated to involve in cardiac remodelling by controlling cardiac fibroblast proliferation and migration. 33 Inhibition of miR-15 family could reduce infarct size and cardiac remodelling and enhance cardiac function in response to MI. 35 Huang et al demonstrated that overexpression of miR-16 could provoke cardiomyocyte hypertrophy by derepressing the cyclins D1, D2 and E1, and activating cyclin/Rb pathway.…”