单位：[1]Huazhong Univ Sci & Technol, Tongji Hosp, Dept Gerontol, Tongji Med Coll, Jie Fang Da Dao 1095, Wuhan 430030, Hubei, Peoples R China综合医疗科华中科技大学同济医学院附属同济医院
Background: RAN guanine nucleotide release factor (RANGRF) encoding protein MOG1 plays an important role in cardiac arrhythmia, so we intended to investigate the regulatory miRNA of RANGRF and explore its potential regulatory mechanism in arrhythmogenesis. Methods: Based on bioinformatic analysis, miR-3144-5p was predicted to be a regulatory miRNA of RANGRF, which were then validated through a dual-luciferase reporter plasmid assay. Subsequently, the expression level of miR-3144-5p in human cardiac myocytes (HCMs) was detected, followed by cell transfection with miR-3144-5p mimics. Transcriptome sequencing was then performed in HCMs with or without transfection. The sequencing results were subjected to bioinformatic analyses, including differentially expressed gene (DEG) analysis, functional enrichment analysis, protein-protein interaction (PPI) network analysis, miRNA-target gene analysis, and miRNA-transcription factor (TF)-target gene coregulatory network analysis. Results: There really existed a regulatory relation between miR-3144-5p and RANGRF. The expression level of miR-3144-5p was low in HCMs. After cell transfection, miR-3144-5p expression level significantly increased in HCMs. Bioinformatic analyses of the transcriptome sequencing results identified 300 upregulated and 271 downregulated DEGs between miR-3144-5p mimic and control group. The upregulated genes ISL1 and neuregulin 1 (NRG1) were significantly enriched in cardiac muscle cell myoblast differentiation (GO: 0060379). CCL21 was one of the hub genes in the PPI network and also a target gene of miR-3144-5p. Moreover, the TF of v-Myc avian myelocytomatosis viral oncogene neuroblastoma-derived homolog (MYCN) was involved in the miR-3144-5p-TF-target gene coregulatory network and interacted with the target genes of miR-3144-5p. Conclusion: ISL1, NRG1, CCL21, and MYCN were differentially expressed in the miR-3144-5p mimic group, suggesting that miR-3144-5p overexpression plays a role in HCMs by regulating these genes and TF. This study may provide new insight into the mechanisms behind the progression of cardiac arrhythmia.
基金：
The independent innovation research fund of Huazhong University of Science and Technology [2017KFYXJJ131]; Specialized Research Fund for the Doctoral Program of Higher Education from the Ministry of Education [20130142120068]
第一作者单位：[1]Huazhong Univ Sci & Technol, Tongji Hosp, Dept Gerontol, Tongji Med Coll, Jie Fang Da Dao 1095, Wuhan 430030, Hubei, Peoples R China
通讯作者：
推荐引用方式(GB/T 7714)：
Ruan Lei,Yang Yi,Huang Yi,et al.Functional prediction of miR-3144-5p in human cardiac myocytes based on transcriptome sequencing and bioinformatics[J].MEDICINE.2017,96(32):doi:10.1097/MD.0000000000007539.
APA：
Ruan, Lei,Yang, Yi,Huang, Yi,Ding, Ling,Zhang, Cuntai&Wu, Xiaofen.(2017).Functional prediction of miR-3144-5p in human cardiac myocytes based on transcriptome sequencing and bioinformatics.MEDICINE,96,(32)
MLA：
Ruan, Lei,et al."Functional prediction of miR-3144-5p in human cardiac myocytes based on transcriptome sequencing and bioinformatics".MEDICINE 96..32(2017)
