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Current Neurovascular Research

Editor-in-Chief

ISSN (Print): 1567-2026
ISSN (Online): 1875-5739

Research Article

MiR-101 Attenuates Myocardial Infarction-induced Injury by Targeting DDIT4 to Regulate Autophagy

Author(s): Qiulan Li, Yanping Gao, Jie Zhu and Qingzhe Jia*

Volume 17, Issue 2, 2020

Page: [123 - 130] Pages: 8

DOI: 10.2174/1567202617666200211113016

Price: $65

Abstract

Background: Myocardial Infarction (MI), a kind of heart deficiency, is the main cause of death and disability. Autophagy, a metabolic process for the degradation of damaged proteins or organelles, is important for cardiac functions and regulated by several miRNAs including miRNA- 101. The aim of this research was to investigate the effects of miR-101 in myocardial infarctioninduced injury and the related mechanisms.

Methods: MI model was induced by ligation of the left coronary artery. The in vitro model was established by hypoxia-induced H9c2 cells (rat myocardial cells). The overexpression of miR-101 was achieved by transfection. The expression of associated proteins was analyzed by Western blotting. The level of miR-101 was analyzed by reverse transcription-polymerase chain reaction (RTPCR). The target genes for miR-101 and the target sites were analyzed by TargetScan.

Results: The results showed that miR-101 was decreased in MI mice (P<0.01). Autophagy and apoptosis were increased in MI-induced injury (in vivo) and in hypoxia treated myocardial cells (in vitro) (P<0.01). miR-101 overexpression inhibited the increase of autophagy and apoptosis in mice and myocardial cells (P<0.01). DDIT4 was a target gene of miR-101 and expressed increasingly in MI-induced injury mice and hypoxia treated myocardial cells. miR-101 could negatively regulate the expression of DDIT4.

Conclusion: This research suggested that miR-101 attenuated- MI-induced injury by targeting DDIT4 to regulate autophagy, which indicated that miR-101 or DDIT4 may be potential therapeutic targets for heart injury.

Keywords: miRNA-101, myocardial infarction-induced injury, DNA damage-inducible transcript 4, autophagy, tissue, heart.

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