MicroRNA-383-5p Regulates Oxidative Stress in Mice with Acute Myocardial Infarction through the AMPK Signaling Pathway via PFKM.

Linlin Gao,Zhongbao Ruan,Gecai Chen,Simona Pichini

doi:10.1155/2021/8587535

Linlin Gao, Zhongbao Ruan + Show 2 more

Open Access

https://doi.org/10.1155/2021/8587535

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Journal: Disease markers	Publication Date: Dec 7, 2021
Citations: 4	License type: CC BY 4.0

Affiliation: Taizhou People's Hospital

Abstract

Objective The purpose of this study is to explore the regulating role of microRNA-383-5p (miR-383-5p) in oxidative stress after acute myocardial infarction (AMI) through AMPK pathway via phosphofructokinase muscle-type (PFKM). Methods We established the AMI model, and the model mice were injected with miR-383-5p agomir to study the effect of miR-383-5p in AMPK signaling pathways. The target gene for miR-383-5p was reported to be PFKM, so we hypothesized that overexpression of miR-383-5p inhibits activation of the AMPK signaling pathway. Results In this research, we found that overexpression of miR-383-5p decreases myocardial oxidative stress, myocardial apoptosis, the expression level of PFKM malondialdehyde (MDA), and reactive oxygen species (ROS) in the myocardial tissues after AMI, and finally, AMI-induced cardiac systolic and diastolic function could be improved.Conclusion This study demonstrated that miR-383-5p could reduce the oxidative stress after AMI through AMPK signaling pathway by targeting PFKM.

Highlights

acute myocardial infarction (AMI) is the main cause of persistent increases in human morbidity and mortality due to obstruction of coronary blood flow [1]
Mice were randomly divided into 4 groups: (1) sham group, (2) AMI+PBS group (AMI mice injected with PBS via tail vein), (3) AMI+miR-383-5p agomir group (AMI mice with miR-383-5p agomir injected via tail vein), and (4) AMI+miR-383-5p agomir NC group (AMI mice with miR-383-5p agomir NC injected via tail vein)
phosphofructokinase muscle-type (PFKM) Can Be Predicted Involving in Regulating the Oxidative Stress

Summary

Objective

The purpose of this study is to explore the regulating role of microRNA-383-5p (miR-383-5p) in oxidative stress after acute myocardial infarction (AMI) through AMPK pathway via phosphofructokinase muscle-type (PFKM). We established the AMI model, and the model mice were injected with miR-383-5p agomir to study the effect of miR-383-5p in AMPK signaling pathways. The target gene for miR-383-5p was reported to be PFKM, so we hypothesized that overexpression of miR-383-5p inhibits activation of the AMPK signaling pathway. We found that overexpression of miR-383-5p decreases myocardial oxidative stress, myocardial apoptosis, the expression level of PFKM malondialdehyde (MDA), and reactive oxygen species (ROS) in the myocardial tissues after AMI, and AMI-induced cardiac systolic and diastolic function could be improved.Conclusion. This study demonstrated that miR-383-5p could reduce the oxidative stress after AMI through AMPK signaling pathway by targeting PFKM

Introduction

Materials and Methods

Results

Discussion