ArticleJournal of the American Heart Association2016
NCK Associated Protein 1 Modulated by miRNA-214 Determines Vascular Smooth Muscle Cell Migration, Proliferation, and Neointima Hyperplasia.
Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
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- A Novel Disulfidptosis-Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy.Journal of cellular and molecular medicine · 2025Article
- Disulfidptosis-Related Genes as Novel Biomarkers and Therapeutic Targets in Dilated Cardiomyopathy.Journal of inflammation research · 2025Article
- GATA2‑miR‑374a axis promotes vascular smooth muscle cells proliferation, migration via targeting circTADA2A/RORA axis.Experimental and therapeutic medicine · 2024Article
- Small nucleolar RNA host gene 18 controls vascular smooth muscle cell contractile phenotype and neointimal hyperplasia.Cardiovascular research · 2024Article
- Disulfidptosis decoded: a journey through cell death mysteries, regulatory networks, disease paradigms and future directions.Biomarker research · 2024Review
- Causal Role for Neutrophil Elastase in Thoracic Aortic Dissection in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Two-Dimensional Polyacrylamide Gel Electrophoresis Coupled with Nanoliquid Chromatography-Tandem Mass Spectrometry-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in the MCF7 Breast Cancer Cell Line Transfected for Jumping Translocation Breakpoint Protein Overexpression.International journal of molecular sciences · 2023Article
- MicroRNA regulation of phenotypic transformations in vascular smooth muscle: relevance to vascular remodeling.Cellular and molecular life sciences : CMLS · 2023Review
- MicroRNA-146a Promotes Embryonic Stem Cell Differentiation towards Vascular Smooth Muscle Cells through Regulation of Kruppel-like Factor 4.Current medical science · 2023Article
- Noncoding RNAs in Vascular Cell Biology and Restenosis.Biology · 2022Review
- Pathogenic role of microRNAs in atherosclerotic ischemic stroke: Implications for diagnosis and therapy.Genes & diseases · 2022Review
- High-content analysis of microRNAs involved in the phenotype regulation of vascular smooth muscle cells.Scientific reports · 2022Article
- Cezanne is a critical regulator of pathological arterial remodelling by targeting β-catenin signalling.Cardiovascular research · 2022Article
- MicroRNA-208a-3p participates in coronary heart disease by regulating the growth of hVSMCs by targeting BTG1.Experimental and therapeutic medicine · 2022Article
- Delivery of miR-654-5p via SonoVue Microbubble Ultrasound Inhibits Proliferation, Migration, and Invasion of Vascular Smooth Muscle Cells and Arterial Thrombosis and Stenosis through Targeting TCF21.Oxidative medicine and cellular longevity · 2022Article
- The Etiology and Molecular Mechanism Underlying Smooth Muscle Phenotype Switching in Intimal Hyperplasia of Vein Graft and the Regulatory Role of microRNAs.Frontiers in cardiovascular medicine · 2022Review
- Relationship of microRNA locus with type 2 diabetes mellitus: a case-control study.Endocrine connections · 2021Article
- Association between microRNA-146a, -499a and -196a-2 SNPs and non-small cell lung cancer: a case-control study involving 2249 subjects.Bioscience reports · 2021Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundMicroRNA miR-214 has been implicated in many biological cellular functions, but the impact of miR-214 and its target genes on vascular smooth muscle cell (VSMC) proliferation, migration, and neointima smooth muscle cell hyperplasia is unknown. METHODS AND
resultsExpression of miR-214 was closely regulated by different pathogenic stimuli in VSMCs through a transcriptional mechanism and decreased in response to vascular injury. Overexpression of miR-214 in serum-starved VSMCs significantly decreased VSMC proliferation and migration, whereas knockdown of miR-214 dramatically increased VSMC proliferation and migration. Gene and protein biochemical assays, including proteomic analyses, showed that NCK associated protein 1 (NCKAP1)-a major component of the WAVE complex that regulates lamellipodia formation and cell motility-was negatively regulated by miR-214 in VSMCs. Luciferase assays showed that miR-214 substantially repressed wild-type but not the miR-214 binding site mutated version of NCKAP1 3' untranslated region luciferase activity in VSMCs. This result confirmed that NCKAP1 is the functional target of miR-214 in VSMCs. NCKAP1 knockdown in VSMCs recapitulates the inhibitory effects of miR-214 overexpression on actin polymerization, cell migration, and proliferation. Data from cotransfection experiments also revealed that inhibition of NCKAP1 is required for miR-214-mediated lamellipodia formation, cell motility, and growth. Importantly, locally enforced expression of miR-214 in the injured vessels significantly reduced NCKAP1 expression levels, inhibited VSMC proliferation, and prevented neointima smooth muscle cell hyperplasia after injury.
conclusionsWe uncovered an important role of miR-214 and its target gene NCKAP1 in modulating VSMC functions and neointima hyperplasia. Our findings suggest that miR-214 represents a potential therapeutic target for vascular diseases.
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