Repositorio UFRO · Omeka S

Long Non-Coding RNAs Might Regulate Phenotypic Switch of Vascular Smooth Muscle Cells Acting as ceRNA: Implications for In-Stent Restenosis

Primer Autor	Salazar, Luis A.
Co-autores	Arencibia, Alberto Lanas, Fernando
Título	Long Non-Coding RNAs Might Regulate Phenotypic Switch of Vascular Smooth Muscle Cells Acting as ceRNA: Implications for In-Stent Restenosis
Editorial	MDPI
Revista	INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Lenguaje	en
Resumen	"Coronary in-stent restenosis is a late complication of angioplasty. It is a multifactorial process that involves vascular smooth muscle cells (VSMCs), endothelial cells, and inflammatory and genetic factors. In this study, the transcriptomic landscape of VSMCs' phenotypic switch process was assessed under stimuli resembling stent injury. Co-cultured contractile VSMCs and endothelial cells were exposed to a bare metal stent and platelet-derived growth factor (PDGF-BB) 20 ng/mL. Migratory capacity (wound healing assay), proliferative capacity, and cell cycle analysis of the VSMCs were performed. RNAseq analysis of contractile vs. proliferative VSMCs was performed. Gene differential expression (DE), identification of new long non-coding RNA candidates (lncRNAs), gene ontology (GO), and pathway enrichment (KEGG) were analyzed. A competing endogenous RNA network was constructed, and significant lncRNA-miRNA-mRNA axes were selected. VSMCs exposed to ""stent injury"" conditions showed morphologic changes, with proliferative and migratory capacities progressing from G0-G1 cell cycle phase to S and G2-M. RNAseq analysis showed DE of 1099, 509 and 64 differentially expressed mRNAs, lncRNAs, and miRNAs, respectively. GO analysis of DE genes showed significant enrichment in collagen and extracellular matrix organization, regulation of smooth muscle cell proliferation, and collagen biosynthetic process. The main upregulated nodes in the lncRNA-mediated ceRNA network were PVT1 and HIF1-AS2, with downregulation of ACTA2-AS1 and MIR663AHG. The PVT1 ceRNA axis appears to be an attractive target for in-stent restenosis diagnosis and treatment."
Tipo de Recurso	artículo original
Description	This research was supported by FONDECYT-ANID, Chile (Grant number 1171765), Direccion de Investigacion-Universidad de La Frontera, Temuco, Chile (Gran Number DI20-0092), and CONICYT Scholarship (Grant number 63140032).
doi	10.3390/ijms23063074
Formato Recurso	PDF
Palabras Claves	long non-coding RNA competing endogenous RNA in-stent restenosis post transcriptional regulation epigenetics transcriptomics in vitro cellular model LNCRNA PVT1 NEOINTIMA FORMATION COCULTURE SYSTEM CORONARY STENT PROLIFERATION ATHEROSCLEROSIS HIF1A-AS2 APOPTOSIS VITRO TRANSCRIPTS
Ubicación del archivo	http://dx.doi.org/10.3390/ijms23063074
Categoría OCDE	Bioquímica y Biología Molecular Química Multidisciplinar
Materias	ARN largo no codificante ARN endógeno competitivo reestenosis en stent regulación postranscripcional epigenética transcriptómica modelo celular in vitro LNCRNA PVT1 FORMACIÓN NEOINTIMA SISTEMA DE COCULTURA STENT CORONARIO PROLIFERACIÓN ATEROSCLEROSIS HIF1A-AS2 APOPTOSIS VITRO TRANSCRIPCIONES
Disciplinas de la OCDE	Sistema Cardiovascular y Cardiaco Biología Molecular Genética Humana
Título de la cita (Recomendado-único)	Long Non-Coding RNAs Might Regulate Phenotypic Switch of Vascular Smooth Muscle Cells Acting as ceRNA: Implications for In-Stent Restenosis
Identificador del recurso (Mandatado-único)	artículo original
Versión del recurso (Recomendado-único)	version publicada
License	CC BY 4.0
Condición de la licencia (Recomendado-repetible)	CC BY 4.0
Derechos de acceso	acceso abierto
Access Rights	acceso abierto
Referencia del Financiador (Mandatado si es aplicable-repetible)	ANID-FONDECYT 1171765 UFRO DI20-0092 CONICYT 63140032 ANID FONDECYT 1171765
Id de Web of Science	WOS:000775241000001