ArticleArteriosclerosis, thrombosis, and vascular biology2013
Myocardin regulates vascular response to injury through miR-24/-29a and platelet-derived growth factor receptor-β.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 50 citations in OpenAlex.
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- Poly(ADP-ribose) polymerase 1 orchestrates vascular smooth muscle cell homeostasis in arterial disease.Experimental & molecular medicine · 2025Article
- Dehydrocorydaline maintains the vascular smooth muscle cell contractile phenotype by upregulating Spta1.Acta pharmacologica Sinica · 2025Article
- Cellular Phenotypic Transformation During Atherosclerosis: The Potential Role of miRNAs as Biomarkers.International journal of molecular sciences · 2025Review
- The Role of MicroRNAs in the Pathogenesis of Doxorubicin-Induced Vascular Remodeling.International journal of molecular sciences · 2024Review
- SMYD2 regulates vascular smooth muscle cell phenotypic switching and intimal hyperplasia via interaction with myocardin.Cellular and molecular life sciences : CMLS · 2023Article
- MicroRNA regulation of phenotypic transformations in vascular smooth muscle: relevance to vascular remodeling.Cellular and molecular life sciences : CMLS · 2023Review
- SMYD2 Regulates Vascular Smooth Muscle Cell Phenotypic Switching and Intimal Hyperplasia via Interaction with Myocardin.Research square · 2023Article
- Transcription factors: key regulatory targets of vascular smooth muscle cell in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2023Review
- Pathophysiology of Atherosclerosis.International journal of molecular sciences · 2022Review
- Versatile role of miR-24/24-1*/24-2* expression in cancer and other human diseases.American journal of translational research · 2022Review
- Surfactant Protein A, a Novel Regulator for Smooth Muscle Phenotypic Modulation and Vascular Remodeling-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Non-coding RNAs: key regulators of smooth muscle cell fate in vascular disease.Cardiovascular research · 2018Review
- Novel Pathological Role of hnRNPA1 (Heterogeneous Nuclear Ribonucleoprotein A1) in Vascular Smooth Muscle Cell Function and Neointima Hyperplasia.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Uremia does not affect neointima formation in mice.Scientific reports · 2017Article
- miR-29a regulates vascular neointimal hyperplasia by targeting YY1.Cell proliferation · 2017Article
- Down-regulation of Insulin Receptor Substrate 1 during Hyperglycemia Induces Vascular Smooth Muscle Cell Dedifferentiation.The Journal of biological chemistry · 2017Article
- Noncoding RNAs in smooth muscle cell homeostasis: implications in phenotypic switch and vascular disorders.Pflugers Archiv : European journal of physiology · 2016Review
- Epigenetic regulation in heart failure.Current opinion in cardiology · 2016Review
- The short and long of noncoding sequences in the control of vascular cell phenotypes.Cellular and molecular life sciences : CMLS · 2015Review
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
objectiveMyocardin, a potent transcriptional coactivator of serum response factor, is involved in vascular development and promotes a contractile smooth muscle phenotype. Myocardin levels are reduced during vascular injury, in association with phenotypic switching of smooth muscle cells (SMCs). However, the direct role of myocardin in vascular disease is unclear. APPROACH AND
resultsWe show that re-expression of myocardin prevents the vascular injury response in murine carotid arteries, with reduced neointima formation due to decreased SMC migration and proliferation. Myocardin reduced SMC migration by downregulating platelet-derived growth factor receptor-β (PDGFRB) expression. Pdgfrb was regulated by myocardin-induced miR-24 and miR-29a expression, and antagonizing these microRNAs restored SMC migration. Furthermore, using miR-24 and miR-29a mimics, we demonstrated that miR-29a directly regulates Pdgfrb expression at the 3' untranslated region while miR-24 has an indirect effect on Pdgfrb levels. Myocardin heterozygous-null mice showed an augmented neointima formation with increased SMC migration and proliferation, demonstrating that endogenous levels of myocardin are a critical regulator of vessel injury responses.
conclusionsOur results extend the function of myocardin from a developmental role to a pivotal regulator of SMC phenotype in response to injury, and this transcriptional coactivator may be an attractive target for novel therapeutic strategies in vascular disease.
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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.