The Role of miRNA-132 against Apoptosis and Oxidative Stress in Heart Failure

Xuelei Liu,Hongxu Jin,Mingxiao Hou,Xiaofang Hu,Zhou Tong,Keyan Chen

doi:10.1155/2018/3452748

Abstract

Objective To explore the effect of microRNA-132 of heart failure and provide theoretical guidance for clinical treatment of heart failure (HF). Methods Peripheral blood was collected from HF patients. RT-qPCR was used to determine microRNA-132 expression. Mouse models of heart failure were established. Color Doppler ultrasound was utilized to measure the changes of cardiac function. HE and Masson staining were applied to observe pathological changes of the myocardium. After H9C2 cells were transfected with microRNA-132, MTT assay was employed to detect the stability of H9C2 cells. ELISA was used to measure the levels of oxidative stress factors. Western blot assay and RT-qPCR were utilized to determine the expression of Bax, Bcl-2, TGF-β1, and smad3. Results MicroRNA-132 expression was downregulated in HF patients' blood. After establishing mouse models of HF, cardiac function obviously decreased. HE staining revealed the obvious edema and hypertrophy of cardiomyocytes. Masson staining demonstrated that cardiomyocytes were markedly fibrotic. After microRNA-132 transfection and H9C2 cell apoptosis induced by H2O2, antioxidant stress and antiapoptotic ability of the H9C2 cells obviously increased. TGF-β1 and smad3 expression remarkably diminished. Conclusion Overexpression of microRNA-132 dramatically increased the antioxidant stress and antiapoptotic ability of H9C2 cells and decreased the expression of TGF-β1 and smad3.

Highlights

Heart failure is a complex set of clinical syndromes, which generates cardiac structure or dysfunction leading to ventricular filling or impaired ejection function [1]
The present study investigated the effect of miRNA-132 in heart failure (HF) models in vivo and in vitro to provide a theoretical basis for targeted therapy of clinical drugs
Real-time fluorescence quantitative PCR results showed that miRNA-132 expression significantly diminished in peripheral blood of HF patients compared with the control group (Figure 1)

Summary

Introduction

Heart failure is a complex set of clinical syndromes, which generates cardiac structure or dysfunction leading to ventricular filling or impaired ejection function [1]. MicroRNA (miRNA) is endogenous noncoding small RNA containing 18–25 nucleotides and is highly conserved during evolution, regulates the gene expression after transcription through sequence-specific interaction of target genes, and participates in many biological processes [3, 4]. MiRNA regulates a single gene, and acts on functionally related gene networks, resulting in complex genetic regulatory networks [5]. Alzahrani et al [6] have found that increased expression of miRNA-132 can reduce the incidence of chronic colitis associated tumors. The present study investigated the effect of miRNA-132 in HF models in vivo and in vitro to provide a theoretical basis for targeted therapy of clinical drugs

Methods

Results

Conclusion