Lei Du1, Zhimin Xu2, Xuhui Wang3, Fang Liu1. 1. Department of Gerontology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200092, P. R. China. 2. Department of Cardiovascular Medicine, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200092, P. R. China. 3. Department of Neurosurgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200092, P. R. China.
Abstract
INTRODUCTION: Coronary artery disease (CAD) is a major global health problem with high incidence and mortality. Despite many advances in treatment, the prognosis of patients with CAD still remains poor. Therefore, this study aimed to identify potential biomarkers and targets associated with the progression of CAD. METHODS: Two gene expression profile datasets (GSE20681 and GSE12288), and two microRNA (miRNA) expression profile datasets (GSE59421 and GSE105449) were downloaded from the Gene Expression Omnibus (GEO) database; R language was used to screen out the differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs), respectively. In addition, five online bioinformatics tools (miRWalk et al.) were used to identify the target genes of DEMs, and miRNA-gene network was constructed using Cytoscape software. Moreover, CCK-8, flow cytometry assays were used to detect the cell proliferation and apoptosis in human umbilical vein endothelial cells (HUVECs). Meanwhile, the dual luciferase reporter system assay was used to explore the interaction of miR-376a-3p and NRIP1 in HUVECs. RESULTS: In the present study, 150 common DEGs and 5 common DEMs were screened using a Venn diagram in R language. First, a total of 6812 target genes were identified from the overlapping DEMs. Second, 26 overlapping dysregulated genes from 150 overlapping DEGs and 6812 miRNA target genes were identified. Meanwhile, 43 miRNA-gene regulatory pairs were obtained between the 5 common DEMs and 26 dysregulated genes. Downregulation of miR-376a-3p significantly inhibited the proliferation of HUVECs via inducing apoptosis. Moreover, overexpression of miR-376a-3p markedly inhibited the growth of HUVECs via downregulating NRIP1. CONCLUSION: In this study, miR-376a-3p-NRIP1 pair might involve in the progression of CAD, implying that miR-376a-3p may be a therapeutic target for the treatment of CAD. AJTR
INTRODUCTION:Coronary artery disease (CAD) is a major global health problem with high incidence and mortality. Despite many advances in treatment, the prognosis of patients with CAD still remains poor. Therefore, this study aimed to identify potential biomarkers and targets associated with the progression of CAD. METHODS: Two gene expression profile datasets (GSE20681 and GSE12288), and two microRNA (miRNA) expression profile datasets (GSE59421 and GSE105449) were downloaded from the Gene Expression Omnibus (GEO) database; R language was used to screen out the differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs), respectively. In addition, five online bioinformatics tools (miRWalk et al.) were used to identify the target genes of DEMs, and miRNA-gene network was constructed using Cytoscape software. Moreover, CCK-8, flow cytometry assays were used to detect the cell proliferation and apoptosis in human umbilical vein endothelial cells (HUVECs). Meanwhile, the dual luciferase reporter system assay was used to explore the interaction of miR-376a-3p and NRIP1 in HUVECs. RESULTS: In the present study, 150 common DEGs and 5 common DEMs were screened using a Venn diagram in R language. First, a total of 6812 target genes were identified from the overlapping DEMs. Second, 26 overlapping dysregulated genes from 150 overlapping DEGs and 6812 miRNA target genes were identified. Meanwhile, 43 miRNA-gene regulatory pairs were obtained between the 5 common DEMs and 26 dysregulated genes. Downregulation of miR-376a-3p significantly inhibited the proliferation of HUVECs via inducing apoptosis. Moreover, overexpression of miR-376a-3p markedly inhibited the growth of HUVECs via downregulating NRIP1. CONCLUSION: In this study, miR-376a-3p-NRIP1 pair might involve in the progression of CAD, implying that miR-376a-3p may be a therapeutic target for the treatment of CAD. AJTR
Authors: Ify R Mordi; Athar A Badar; R John Irving; Jonathan R Weir-McCall; J Graeme Houston; Chim C Lang Journal: Vasc Health Risk Manag Date: 2017-11-21
Authors: Alipio Mangas; Alexandra Pérez-Serra; Fernando Bonet; Ovidio Muñiz; Francisco Fuentes; Aurora Gonzalez-Estrada; Oscar Campuzano; Juan Sebastian Rodriguez Roca; Elena Alonso-Villa; Rocio Toro Journal: Int J Mol Sci Date: 2022-07-24 Impact factor: 6.208
Authors: Sajad Najafi; Soudeh Ghafouri-Fard; Bashdar Mahmud Hussen; Hazha Hadayat Jamal; Mohammad Taheri; Mohammad Hallajnejad Journal: Front Cell Dev Biol Date: 2022-01-17