The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy.

Mailin Gan,Yuan Fan,Shunhua Zhang,Dongmei Jiang,Lin Bai,Lei Chen,Linyuan Shen,Li Zhu,Ya Tan,Zhixian Guo,Xiaoxia Hao,Xuewei Li

doi:10.3390/cells9051173

Abstract

Cardiac hypertrophy is a common pathological condition and an independent risk factor that triggers cardiovascular morbidity. As an important epigenetic regulator, miRNA is widely involved in many biological processes. In this study, miRNAs expressed in rat hearts that underwent isoprenaline-induced cardiac hypertrophy were identified using high-throughput sequencing, and functional verification of typical miRNAs was performed using rat primary cardiomyocytes. A total of 623 miRNAs were identified, of which 33 were specifically expressed in cardiac hypertrophy rats. The enriched pathways of target genes of differentially expressed miRNAs included the FoxO signaling pathway, dopaminergic synapse, Wnt signaling pathway, MAPK (mitogen-activated protein kinase) signaling pathway, and Hippo signaling pathway. Subsequently, miR-144 was the most differentially expressed miRNA and was subsequently selected for in vitro validation. Inhibition of miR-144 expression in primary myocardial cells caused up-regulation of cardiac hypertrophy markers atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The dual luciferase reporter system showed that ANP may be a target gene of miR-144. Long non-coding RNA myocardial infarction associated transcript (LncMIAT) is closely related to heart disease, and here, we were the first to discover that LncMIAT may act as an miR-144 sponge in isoproterenol-induced cardiac hypertrophy. Taken together, these results enriched the understanding of miRNA in regulating cardiac hypertrophy and provided a reference for preventing and treating cardiac hypertrophy.

Highlights

IntroductionCardiac hypertrophy is a powerful type of compensation, if the cause cannot be eliminated for a prolonged period of time, the function of the hypertrophic myocardium cannot remain normal for a long time and eventually turns to heart failure [2]
Cardiac hypertrophy is a compensatory response of the heart to provide normal cardiac output under a variety of cardiovascular diseases, including hypertension and coronary heart disease [1]. cardiac hypertrophy is a powerful type of compensation, if the cause cannot be eliminated for a prolonged period of time, the function of the hypertrophic myocardium cannot remain normal for a long time and eventually turns to heart failure [2]
We focused on the possible functional role of miRNAs in ISO-induced cardiac hypertrophy

Summary

Introduction

Cardiac hypertrophy is a powerful type of compensation, if the cause cannot be eliminated for a prolonged period of time, the function of the hypertrophic myocardium cannot remain normal for a long time and eventually turns to heart failure [2]. Cardiac hypertrophy involves a variety of pathophysiological signals, such as physical, chemical, and hormonal levels, including angiotensin II (Ang II), norepinephrine and beta-adrenergic receptor agonists [4,5]. Previous studies have shown that ISO can trigger cardiac hypertrophy by activating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) [8]. ANP and BNP are secreted in large amounts [11]. ANP and BNP are often used as markers of cardiac hypertrophy [12]

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Conclusion