Transcription Factors Targeted by miRNAs Regulating Smooth Muscle Cell Growth and Intimal Thickening after Vascular Injury

Neointima formation after percutaneous coronary intervention (PCI) is a manifestation of "phenotype switching" by vascular smooth muscle cells (SMC), a process that involves de-differentiation from a contractile quiescent phenotype to one that is richly synthetic. In response to injury, SM...

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Bibliographic Details
Published in:International journal of molecular sciences 2019-10, Vol.20 (21), p.5445
Main Author: Khachigian, Levon M
Format: Article
Language:English
Subjects:
Animals
Atherosclerosis
Binding sites
Biosynthesis
c-Myb protein
Cardiovascular disease
Carotid arteries
Cells, Cultured
Differentiation
EGR-1 protein
FOXO4 protein
Gene expression
Gene Expression Regulation
Genes
Genotype & phenotype
HMGB1 protein
Humans
Hyperplasia
Hypertension
immediate-early genes
Immediate-early proteins
intimal thickening
JunB protein
KLF4 protein
MicroRNAs - genetics
miRNA
Muscle contraction
Muscles
Myocytes, Smooth Muscle - metabolism
Neointima - genetics
neointima formation
Non-coding RNA
Percutaneous Coronary Intervention - adverse effects
Phenotypes
Proteins
Review
Smad3 protein
Smooth muscle
smooth muscle cells
Sp1 protein
Stents
Thickening
Transcription factors
Transcription Factors - genetics
Vascular System Injuries - etiology
Vascular System Injuries - genetics
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Summary:Neointima formation after percutaneous coronary intervention (PCI) is a manifestation of "phenotype switching" by vascular smooth muscle cells (SMC), a process that involves de-differentiation from a contractile quiescent phenotype to one that is richly synthetic. In response to injury, SMCs migrate, proliferate, down-regulate SMC-specific differentiation genes, and later, can revert to the contractile phenotype. The vascular response to injury is regulated by microRNAs (or miRNAs), small non-coding RNAs that control gene expression. Interactions between miRNAs and transcription factors impact gene regulatory networks. This article briefly reviews the roles of a range of miRNAs in molecular and cellular processes that control intimal thickening, focusing mainly on transcription factors, some of which are encoded by immediate-early genes. Examples include Egr-1, junB, KLF4, KLF5, Elk-1, Ets-1, HMGB1, Smad1, Smad3, FoxO4, SRF, Rb, Sp1 and c-Myb. Such mechanistic information could inform the development of strategies that block SMC growth, neointima formation, and potentially overcome limitations of lasting efficacy following PCI.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms20215445