ArticleArteriosclerosis, thrombosis, and vascular biology2011
Induction of microRNA-1 by myocardin in smooth muscle cells inhibits cell proliferation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 135 citations in OpenAlex.
- miRNA in the Diagnosis and Treatment of Critical Limb Ischemia.Biomedicines · 2024Article
- Long non-coding RNAs in cardiac hypertrophy and heart failure: functions, mechanisms and clinical prospects.Nature reviews. Cardiology · 2024Review
- Pim Kinases: Important Regulators of Cardiovascular Disease.International journal of molecular sciences · 2023Review
- MicroRNA regulation of phenotypic transformations in vascular smooth muscle: relevance to vascular remodeling.Cellular and molecular life sciences : CMLS · 2023Review
- Role of miRNAs in vascular development.Non-coding RNA research · 2023Review
- Transcription factors: key regulatory targets of vascular smooth muscle cell in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2023Review
- Epigenetic modifications as therapeutic targets in atherosclerosis: a focus on DNA methylation and non-coding RNAs.Frontiers in cardiovascular medicine · 2023Review
- Non-Coding RNAs in Regulating Plaque Progression and Remodeling of Extracellular Matrix in Atherosclerosis.International journal of molecular sciences · 2022Review
- SENP2 Promotes VSMC Phenotypic Switching via Myocardin De-SUMOylation.International journal of molecular sciences · 2022Article
- Targeting the phenotypic switch of vascular smooth muscle cells to tackle atherosclerosis.Atherosclerosis · 2021Article
- Plasma Small Extracellular Vesicle-Carried miRNA-501-5p Promotes Vascular Smooth Muscle Cell Phenotypic Modulation-Mediated In-Stent Restenosis.Oxidative medicine and cellular longevity · 2021Article
- Epigenetic Regulation of Vascular Smooth Muscle Cell Phenotype Switching in Atherosclerotic Artery Remodeling: A Mini-Review.Frontiers in genetics · 2021Review
- Targeting hyperactive TGFBR2 for treating MYOCD deficient lung cancer.Theranostics · 2021Article
- Article
- miR-182-3p/Myadm contribute to pulmonary artery hypertension vascular remodeling via a KLF4/p21-dependent mechanism.Theranostics · 2020Article
- MicroRNAs as Therapeutic Targets and Clinical Biomarkers in Atherosclerosis.Journal of clinical medicine · 2019Review
- The microRNAs Regulating Vascular Smooth Muscle Cell Proliferation: A Minireview.International journal of molecular sciences · 2019Review
- MicroRNA-1-Mediated Inhibition of Cardiac Fibroblast Proliferation Through Targeting Cyclin D2 and CDK6.Frontiers in cardiovascular medicine · 2019Article
- TNF-α elicits phenotypic and functional alterations of vascular smooth muscle cells by miR-155-5p-dependent down-regulation of cGMP-dependent kinase 1.The Journal of biological chemistry · 2018Article
- Impact of miRNA in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2018Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
objectiveMyocardin is a cardiac- and smooth muscle-specific transcription co-factor that potently activates the expression of downstream target genes. Previously, we demonstrated that overexpression of myocardin inhibited the proliferation of smooth muscle cells (SMCs). Recently, myocardin was reported to induce the expression of microRNA-1 (miR-1) in cardiomyocytes. In this study, we investigated whether myocardin induces miR-1 expression to mediate its inhibitory effects on SMC proliferation. METHODS AND
resultsUsing tetracycline-regulated expression (T-REx) inducible system expressing myocardin in human vascular SMCs, we found that overexpression of myocardin resulted in significant induction of miR-1 expression and inhibition of SMC proliferation, which was reversed by miR-1 inhibitors. Consistently, introduction of miR-1 into SMCs inhibited their proliferation. We isolated spindle-shaped and epithelioid human SMCs and demonstrated that spindle-shaped SMCs were more differentiated and less proliferative. Correspondingly, spindle-shaped SMCs had significantly higher expression levels of both myocardin and miR-1 than epithelioid SMCs. We identified Pim-1, a serine/threonine kinase, as a target gene for miR-1 in SMCs. Western blot and luciferase reporter assays further confirmed that miR-1 targeted Pim-1 directly. Furthermore, neointimal lesions of mouse carotid arteries displayed downregulation of myocardin and miR-1 with upregulation of Pim-1.
conclusionsOur data demonstrate that miR-1 participates in myocardin-dependent of SMC proliferation inhibition.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.