Dataset Information

Bioinformatic Analysis of the Possible Regulative Network of miR-30a/e in Cardiomyocytes 2 Days Post Myocardial Infarction.

ABSTRACT: Background:Both miR-30a and miR-30e are significantly downregulated in cardiomyocytes (CMs) 2 days (d) post myocardial infarction (MI). This study aimed to identify their possible regulative network in CMs 2d post-MI. Methods:The dysregulated mRNAs in left ventricle tissues 2d post-MI in mice model were retrieved from one previous publication. The verified target genes of miR-30a/e and the predicted targets (upregulated 2d post-MI) were subjected to analysis of the involvement in biological processes according to their enrichment in gene ontology (GO) terms. Results:The known targets of miR-30a/e can regulate cellular responses to glucose starvation via targeting TP53, BECH1 and HSPA5, and also control cardiac epithelial to mesenchymal transition via targeting ETS-related gene (ERG), SNAI1 and NOTCH1. Bioinformatic prediction further showed that miR-30a might regulate some biological processes related to CM responses to MI via some other potential targets, such as platelet aggregation (possibly via ITGB3 and STXBP1), regulation of intrinsic apoptotic signaling pathway in response to deoxyribonucleic acid damage (possibly via SNAI1) and positive regulation of tyrosine phosphorylation of Stat3 protein (possibly via LYN, SOCS3 and SLCF1). Conclusions:Considering the importance of these genes in cellular responses to MI, it is meaningful to further investigate the regulative effect of miR-30a/e on their expression, as well as their regulative network in CMs.

SUBMITTER: Wang Y

PROVIDER: S-EPMC5863072 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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Bioinformatic Analysis of the Possible Regulative Network of miR-30a/e in Cardiomyocytes 2 Days Post Myocardial Infarction.

Wang Yiping Y Huang Yingqiong Y Zhang Min M Zhang Xiaoqin X Tang Xuemei X Kang Yan Y

Acta Cardiologica Sinica 20180301 2

<h4>Background</h4>Both miR-30a and miR-30e are significantly downregulated in cardiomyocytes (CMs) 2 days (d) post myocardial infarction (MI). This study aimed to identify their possible regulative network in CMs 2d post-MI.<h4>Methods</h4>The dysregulated mRNAs in left ventricle tissues 2d post-MI in mice model were retrieved from one previous publication. The verified target genes of miR-30a/e and the predicted targets (upregulated 2d post-MI) were subjected to analysis of the involvement in ...[more]

PMID: 29643704

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Project description:BackgroundMitochondrial dysfunction has been implicated in the pathogenesis of ischemic heart disease, exacerbating cardiomyocytes injury in myocardial infarction (MI). Peroxisome proliferator-activated receptor gamma co-activator (PGC-1?) has been recognized as the key regulator of mitochondrial biogenesis and energy metabolism. Yiqihuoxue decoction (YQHX), a Traditional Chinese Medicine (TCM) prescription, can prevent and treat ischemic heart disease. However, the mechanisms of YQHX on PGC-1? expression in the ischemic heart have remained unclear.MethodsMyocardial ischemia rat model and ischemia/hypoxia injury model in the cardiomyocytes were used to minic human cardiovascular disease. Rats were randomly assigned into 4 groups: Sham, Model, YQHX (8.2 g/kg) and Trimetazidine (10 mg/kg) group. 28 days after MI, cardiac functions and morphology were detected by echocardiography and HE staining, respectively. In vitro, the effects of YQHX on H9c2 cell viability, LDH and ROS were detected, respectively. PGC-1? relevant proteins were evaluated by Western blotting.ResultsIn vivo, echocardiography and HE staining results showed that YQHX improved cardiac functions and modified pathological changes. YQHX enhanced PGC-1? expression and improved the mitochondrial ultrastructure and functions in rats MI model for 4 weeks. Further, we explored its potential mechanisms in cardiomyocytes. In vitro, YQHX significantly enhanced cell viability and reduced LDH release and ROS production induced by hypoxia in cardiomyocytes. Interestingly, exposure of cardiomyocytes to hypoxic conditions for 12 h induced the downregulation of PGC-1? expression, but the expression levels nearly returned to the normal state after hypoxia for 24 h. YQHX significantly enhanced PGC-1? expression between 12 h and 24 h induced by hypoxia through a mechanism associated with the activation of AMPK phosphorylation in H9c2 cells. In addition, YQHX upregulated the expression of Tfam and NRF-1, while NRF-1 expression was completely blocked by an AMPK inhibitor. YQHX largely restored the mitochondrial morphology and increased mitochondrial membrane potential in hypoxia-induced injury. Furthermore, the UHPLC-LTQ-Orbitrap-MSn analysis found that there were 87 chemical constituents in YQHX.ConclusionsThese results suggest that the protective effect of YQHX on cardiomyocytes against hypoxia-induced injury may be attributed to activation of PGC-1? and maintenance of mitochondrial functions through a mechanism involving the activation of AMPK phosphorylation.

Dataset Information

Bioinformatic Analysis of the Possible Regulative Network of miR-30a/e in Cardiomyocytes 2 Days Post Myocardial Infarction.

Publications

Bioinformatic Analysis of the Possible Regulative Network of miR-30a/e in Cardiomyocytes 2 Days Post Myocardial Infarction.

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