ArticlePloS one2010
Chromatin remodeling pathways in smooth muscle cell differentiation, and evidence for an integral role for p300.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- P300 in Inflammation: An Updated Perspective on Its Molecular Mechanisms and Therapeutic Potential.Inflammation · 2026Review
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
- CBX1 as a Prognostic Biomarker and Therapeutic Target in Liver Hepatocellular Carcinoma: Insight into DNA Methylation and Non-Coding RNA Networks from Comprehensive Bioinformatics Analysis.Medicina (Kaunas, Lithuania) · 2025Article
- Nuclear Control of Vascular Smooth Muscle Cell Plasticity during Vascular Remodeling.The American journal of pathology · 2024Review
- Somatic Variants in SVIL in Cerebral Aneurysms.Neurology. Genetics · 2022Article
- Histone Acetyltransferases p300 and CBP Coordinate Distinct Chromatin Remodeling Programs in Vascular Smooth Muscle Plasticity.Circulation · 2022Article
- Early Programming of Adult Systemic Essential Hypertension.International journal of molecular sciences · 2020Review
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- Epigenetic regulation of vascular smooth muscle cell function in atherosclerosis.Current atherosclerosis reports · 2013Review
- Mechanical regulation of epigenetics in vascular biology and pathobiology.Journal of cellular and molecular medicine · 2013Review
- Article
- Vascular smooth muscle cell phenotypic plasticity: focus on chromatin remodelling.Cardiovascular research · 2012Review
- Epigenetic modifications in cardiovascular disease.Basic research in cardiology · 2012Review
- The virtue of just enough stress: a molecular model.Transactions of the American Clinical and Climatological Association · 2012Article
- Ghrelin O-acyltransferase assays and inhibition.Methods in enzymology · 2012Review
- Smooth muscle cell differentiation in vitro: models and underlying molecular mechanisms.Arteriosclerosis, thrombosis, and vascular biology · 2011Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPhenotypic alteration of vascular smooth muscle cells (SMC) in response to injury or inflammation is an essential component of vascular disease. Evidence suggests that this process is dependent on epigenetic regulatory processes. P300, a histone acetyltransferase (HAT), activates crucial muscle-specific promoters in terminal (non-SMC) myocyte differentiation, and may be essential to SMC modulation as well.
resultsWe performed a subanalysis examining transcriptional time-course microarray data obtained using the A404 model of SMC differentiation. Numerous chromatin remodeling genes (up to 62% of such genes on our array platform) showed significant regulation during differentiation. Members of several chromatin-remodeling families demonstrated involvement, including factors instrumental in histone modification, chromatin assembly-disassembly and DNA silencing, suggesting complex, multi-level systemic epigenetic regulation. Further, trichostatin A, a histone deacetylase inhibitor, accelerated expression of SMC differentiation markers in this model. Ontology analysis indicated a high degree of p300 involvement in SMC differentiation, with 60.7% of the known p300 interactome showing significant expression changes. Knockdown of p300 expression accelerated SMC differentiation in A404 cells and human SMCs, while inhibition of p300 HAT activity blunted SMC differentiation. The results suggest a central but complex role for p300 in SMC phenotypic modulation.
conclusionsOur results support the hypothesis that chromatin remodeling is important for SMC phenotypic switching, and detail wide-ranging involvement of several epigenetic modification families. Additionally, the transcriptional coactivator p300 may be partially degraded during SMC differentiation, leaving an activated subpopulation with increased HAT activity and SMC differentiation-gene specificity.
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