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Abstract
Myocardial infarction (MI) is a leading cause of death in the world and many genes are involved in it. Transcription factor (TFs) and microRNAs (miRNAs) are key regulators of gene expression. We hypothesized that miRNAs and TFs might play combinatory regulatory roles in MI. After collecting MI candidate genes and miRNAs from various resources, we constructed a comprehensive MI-specific miRNA-TF co-regulatory network by integrating predicted and experimentally validated TF and miRNA targets. We found some hub nodes (e.g. miR-16 and miR-26) in this network are important regulators, and the network can be severed as a bridge to interpret the associations of previous results, which is shown by the case of miR-29 in this study. We also constructed a regulatory network for MI recurrence and found several important genes (e.g. DAB2, BMP6, miR-320 and miR-103), the abnormal expressions of which may be potential regulatory mechanisms and markers of MI recurrence. At last we proposed a cellular model to discuss major TF and miRNA regulators with signaling pathways in MI. This study provides more details on gene expression regulation and regulators involved in MI progression and recurrence. It also linked up and interpreted many previous results.
Highlights
IntroductionTranscription factors (TFs) are paramount regulators of gene expression in living organisms[17], and play important roles in Myocardial infarction (MI)
Hubei Bioinformatics & Molecular Imaging Key Laboratory, Department of Biomedical Engineering, Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China
We investigated the feed-forward loops (FFLs) and feedback loops among these genes, and constructed the miRNA-Transcription factors (TFs) co-regulatory network in Myocardial infarction (MI) as described in the Methods section and Supplementary Fig. S1
Summary
Transcription factors (TFs) are paramount regulators of gene expression in living organisms[17], and play important roles in MI. Such as EGR1, ATF3, ATF4, MYC and FOS were considered as the key TFs related to the development of AMI18. TF and miRNA may mutually regulate each www.nature.com/scientificreports another forming feedback loops (FBLs), or regulate a shared target gene to form feed-forward loops (FFLs)[11,19,20] Both miRNAmediated FBLs and FFLs are significant and recurrent network motifs, which play important roles in gene regulation in mammalian genomes[21,22].
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