Identification and function analysis of differentially expressed miRNAs in rat myocardial infarction model
10.3969/j.issn.1001-1978.2021.05.015
- Author:
Dao-Min YAO
1
;
Jing ZHU
1
;
Liang XIE
2
;
Jian-Bin GONG
2
;
Jing LIU
2
Author Information
1. School of Pharmacy, Nanjing University of Chinese Medicine
2. Dept of Cardiology, Jinling Hospital, Medical School of Nanjing University
- Publication Type:Journal Article
- Keywords:
bioinformatics;
expression profiles;
long non-coding RNA;
MicroRNA;
mRNA;
myocardial infarction
- From:
Chinese Pharmacological Bulletin
2021;37(5):673-680
- CountryChina
- Language:Chinese
-
Abstract:
Aim To identify differentially expressed microRNAs (miRNAs) in rat myocardial infarcted tissues and predict their interaction with IncRNAs and target genes, as well as to explore potential pathophysiology mechanisms in myocardial infarction. Methods A rat model of myocardial infarction was established by ligating the left anterior descending coronary artery. Trizolwas used to extract total RNA from infarcted myocardial area for microarray detection. Bioinformatics methods were used to predict interaction IncRNAs, target genes, and functional enrichment of miRNAs thatwere significantly differently expressed. The possible IncRNA-miRNA-mRNA regulatory networks were identified finally. Results The elevation of ST segment of ECG showed that the rat model of myocardial infarction was successfully prepared. Microarray results showed that there were 19 significantly differently expressed miRNAs. Eight of these miRNAs (miR-21, miR-132, miR-222, miR-223-3p, miR-146a/b, miR-181b, miR-449a-5p, miR-122) were proven to be myocardial infarction treatment candidates. Whether seven miR-NAs (miR-365-5p, miR490-5p, miR-6333, miR-30cl-3p, miR-3591, miR-3596c, miR-877) were related to myocardial infarction called for further confirmation. There might be several new IncRNA-miRNA-mRNA mechanisms in the development of myocardial infarction. ENSRNOT00000076620-miR-146b-5p-STAT3/Rnf7/Qrsll may be involved in the process of cardiomyocyte apoptosis and mitochondrial damage during myocardial infarction. ENSRNOT00000071991-miR-122-Deptor might inhibit the autophagy of cardiomyocytes and exacerbate myocardial infarction. Conclusions The ternary relationship of IncRNA-miRNA-mRNA obtained in this study may provide possible research directions and a certain theoretical basis for further exploration of the molecular level pathological mechanism of myocardial infarction, and new therapeutic targets for myocardial infarction as well.
