Microarray analysis of the time-dependent expression profiles of long non-coding RNAs in the progression of vein graft stenotic disease

xlomafota13 shared this article with you from Inoreader Microarray analysis of the time-dependent expression profiles of long non-coding RNAs in the progression of vein graft stenotic disease Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jun;21(6):635. doi: 10.3892/etm.2021.10067. Epub 2021 Apr 15. ABSTRACT Long non-coding RNAs (lncRNAs) have been reported to be involved in various biological processes, including cell proliferation and apoptosis. However, the expression profiles of lncRNAs in patients with vein graft restenosis remain unknown. In the present study, the time-dependent expression profiles of genes in vein bypass grafting models were examined by microarray analysis. A total of 2,572 lncRNAs and 1,652 mRNAs were identified to be persistently significantly differentially expressed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis was performed to investigate the functions of these lncRNAs. A total of 360 lncRNAs and 135 protein-coding genes were predicted to be involved in the vascular remodeling process. Co-expression network analysis revealed the association between 194 lncRNAs and seven associated protein-c oding genes, including transforming growth factor-β1, Fes, Yes1 associated transcriptional regulator, sphingosine-1-phosphate receptor 1, Src, insulin receptor and melanoma cell adhesion molecule. Moreover, reverse transcription-quantitative PCR results supported those of the microarray data, and overexpression of AF062402, which regulates the transcription of Src, stimulated the proliferation of primary vascular smooth muscle cells. The findings of the present study may facilitate the development of novel therapeutic targets for vein graft restenosis and may help to improve the prognosis of patients following coronary artery bypass grafting. PMID:33968166 | PMC:PMC8097238 | DOI:10.3892/etm.2021.10067 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.