Wang Yiping, Huang Yingqiong, Zhang Min, Zhang Xiaoqin, Tang Xuemei, Kang Yan
Intensive Care Unit, West China Hospital, Sichuan University, Chengdu, 610041.
Intensive Care Unit.
Acta Cardiol Sin. 2018 Mar;34(2):175-188. doi: 10.6515/ACS.201803_34(2).20170926A.
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.
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.
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).
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.
在心肌梗死(MI)后2天,miR - 30a和miR - 30e在心肌细胞(CMs)中均显著下调。本研究旨在确定它们在MI后2天的CMs中可能的调控网络。
从小鼠模型MI后2天的左心室组织中检索失调的mRNA。根据miR - 30a/e的已验证靶基因和预测靶标(MI后2天上调)在基因本体(GO)术语中的富集情况,对它们参与生物过程进行分析。
miR - 30a/e的已知靶标可通过靶向TP53、BECH1和HSPA5来调节细胞对葡萄糖饥饿的反应,还可通过靶向ETS相关基因(ERG)、SNAI1和NOTCH1来控制心脏上皮向间充质转化。生物信息学预测进一步表明,miR - 30a可能通过一些其他潜在靶标调节与CM对MI反应相关的一些生物过程,如血小板聚集(可能通过ITGB3和STXBP1)、对脱氧核糖核酸损伤的内源性凋亡信号通路调节(可能通过SNAI1)以及Stat3蛋白酪氨酸磷酸化的正调控(可能通过LYN、SOCS3和SLCF1)。
考虑到这些基因在细胞对MI反应中的重要性,进一步研究miR - 30a/e对其表达的调控作用以及它们在CMs中的调控网络具有重要意义。