MiR-106b and MiR-15b Modulate Apoptosis and Angiogenesis in Myocardial Infarction

Cellular Physiology and Biochemistry

关键词: Myocardial infarction;    MicroRNA;    Bioinformatics;    Regulatory network;    Apoptosis;    Angiogenesis;   

DOI  :  10.1159/000258197

学科分类：分子生物学，细胞生物学和基因

来源: S Karger AG

【 摘 要 】

Background MicroRNAs (miRNAs) are identified as crucial gene regulators in response to myocardial infarction (MI). However, the overall relationships between miRNAs and the gene targets which contribute to the cellular phenotypes in MI are not fully elucidated. To make a better understanding towards functional roles of miRNAs in MI, useful information was mined through bioinformatic techniques. Method MI-related miRNAs were retrieved from publications, and PicTar, TargetScanS, and miRanda programs were used to predict their gene targets. Gene ontology (GO) and pathway analyses of gene targets were applied to uncover functional roles of miRNAs. The miRNA-gene networks were illustrated by Pajek tool. Finally, validation experiments were performed towards two important miRNAs in the networks. Result Up to 119 MI-related miRNAs were retrieved from publications. GO and pathway analyses for their predicted gene targets demonstrated that these dysregulated miRNAs were enriched in cardiovascular-related phenotypes. Through illustrating miRNA-gene networks, overall relationships between miRNAs and gene targets were detected especially in processes of apoptosis and angiogenesis. Moreover, experimental data supported bioinformatic predictions that miR-106b served as an anti-apoptotic modulator through inhibition of p21 expression and miR-15b displayed anti-angiogenesis activity. Conclusion The miRNAs played essential roles in pathological processes of MI. Further, miR-106b and miR-15b maybe mediated as robust regulators in apoptosis or angiogenesis following MI, respectively.

【 授权许可】

CC BY-NC-ND