EXPERIMENTAL RESEARCH
MiR-200a promotes the survival of cardiac cells and improves cardiac injury in chronic heart failure rats
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1
Department of Cardiology, Shanxi Provincial People’s Hospital, Taiyuan, Shanxi, China
2
Department of AIDS Prevention and Control, Taiyuan Center for Disease Control and Prevention, Taiyuan, Shanxi, China
Submission date: 2020-02-22
Final revision date: 2020-03-10
Acceptance date: 2020-03-12
Online publication date: 2020-04-19
 
 
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ABSTRACT
Introduction:
miRNAs play an important role in cardiovascular abnormalities such as heart failure. In the present work we evaluated the role of miR-200a in the condition of chronic heart failure and also the mechanism involved.

Material and methods:
In the study 180 subjects, among whom 100 were reported for chronic heart failure and 80 as normal, were included. ELISA and qRT-PCR was done to evaluate levels of HMGB1 and miR-200a in subjects. The cardiac hemodynamics and functioning, oxidative stress and expression of mediators of inflammation were studied in rats with chronic heart failure induced after transfecting them with miR-200a or HMGB1. Luciferase activity was measured to establish any correlation between HMGB1 and miR-200a.

Results:
The chronic heart failure patients included in the study showed suppressed levels of miR-200a and elevated HMGB1 compared to normal subjects. In chronic heart failure rats, the transfection of miR-200a attenuated the cardiac function and other hemodynamic parameters. In addition, improvement in oxidative stress as well as inflammatory mediators was observed. The outcomes also confirmed that HMGB1 was the potential target of miR-200a. It was also noted that upon transfection miR-200a resulted in suppression of protein as well as mRNA levels of HMGB1 in the cardiac tissue of chronic heart failure rats. Also overexpression of HMGB1 decreased the effects of miR-200a.

Conclusions:
The outcomes indicate that miR-200a exerts a protective effect on cardiac cell injury via the HMGB1 pathway.

eISSN:1896-9151
ISSN:1734-1922