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
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
Colecciones
Colección Publicaciones Científicas
Colección ANID
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