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Updated: May 22, 2026
Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
MiR-106b and MiR-15b modulate apoptosis and angiogenesis in myocardial infarction
Zhihua Liu1, Dan Yang, Ping Xie
1Center for Computational Biology and Bioinformatics, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. zhliu@implad.ac.cn
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.
Insights
MicroRNAs (miRNAs) regulate genes in myocardial infarction (MI). This study identified key miRNAs and their targets involved in apoptosis and angiogenesis, revealing miR-106b and miR-15b as crucial regulators in MI.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Bioinformatics
Background:
- MicroRNAs (miRNAs) are critical regulators of gene expression following myocardial infarction (MI).
- The precise roles and interactions of miRNAs in MI-related cellular phenotypes remain incompletely understood.
- Bioinformatic approaches are essential for elucidating miRNA functions in MI pathogenesis.
Purpose of the Study:
- To comprehensively identify microRNAs (miRNAs) associated with myocardial infarction (MI).
- To predict and analyze the gene targets of MI-related miRNAs.
- To understand the functional roles of miRNAs in MI through network analysis and experimental validation.
Main Methods:
- Systematic retrieval of MI-related miRNAs from scientific literature.
- Prediction of miRNA gene targets using bioinformatic tools (PicTar, TargetScanS, miRanda).
- Gene Ontology (GO) and pathway analyses to determine functional enrichment; network visualization using Pajek; experimental validation of key miRNAs.
Main Results:
- 119 MI-related miRNAs were identified, with predicted targets enriched in cardiovascular-related pathways.
- miRNA-gene network analysis highlighted roles in apoptosis and angiogenesis.
- Experimental validation confirmed miR-106b's anti-apoptotic function (via p21 inhibition) and miR-15b's anti-angiogenic activity.
Conclusions:
- MicroRNAs play significant roles in the pathological processes of myocardial infarction.
- miR-106b and miR-15b emerge as potent regulators of apoptosis and angiogenesis, respectively, in the context of MI.
