ArticleMolecular and cellular biology2005
Smooth muscle-specific genes are differentially sensitive to inhibition by Elk-1.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 68 citations in OpenAlex.
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
- Review
- SRF SUMOylation modulates smooth muscle phenotypic switch and vascular remodeling.Nature communications · 2024Article
- Cardiac pericyte reprogramming by MEK inhibition promotes arteriologenesis and angiogenesis of the ischemic heart.The Journal of clinical investigation · 2022Article
- Serum response factor-cofactor interactions and their implications in disease.The FEBS journal · 2021Review
- The Aftermath of Bronchoconstriction.Journal of engineering and science in medical diagnostics and therapy · 2019Review
- PEA-15 (Phosphoprotein Enriched in Astrocytes 15) Is a Protective Mediator in the Vasculature and Is Regulated During Neointimal Hyperplasia.Journal of the American Heart Association · 2017Article
- Elastic, silk-cardiac extracellular matrix hydrogels exhibit time-dependent stiffening that modulates cardiac fibroblast response.Journal of biomedical materials research. Part A · 2016Article
- Forkhead box F2 regulation of platelet-derived growth factor and myocardin/serum response factor signaling is essential for intestinal development.The Journal of biological chemistry · 2015Article
- Caveolin-3 Promotes a Vascular Smooth Muscle Contractile Phenotype.Frontiers in cardiovascular medicine · 2015Article
- Downregulated protein expression of transcriptional activator ELK-1 in atrial myocardium of chronic AF patients.International journal of clinical and experimental pathology · 2015Article
- The transcription factor TEAD1 represses smooth muscle-specific gene expression by abolishing myocardin function.The Journal of biological chemistry · 2014Article
- TGF-β/Smad3 stimulates stem cell/developmental gene expression and vascular smooth muscle cell de-differentiation.PloS one · 2014Article
- The transcription factor Foxf1 binds to serum response factor and myocardin to regulate gene transcription in visceral smooth muscle cells.The Journal of biological chemistry · 2013Article
- Smooth muscle-selective inhibition of nuclear factor-κB attenuates smooth muscle phenotypic switching and neointima formation following vascular injury.Journal of the American Heart Association · 2013Article
- Kruppel-like factor 4 contributes to high phosphate-induced phenotypic switching of vascular smooth muscle cells into osteogenic cells.The Journal of biological chemistry · 2012Article
- Yap1 protein regulates vascular smooth muscle cell phenotypic switch by interaction with myocardin.The Journal of biological chemistry · 2012Article
- Signaling mechanisms that regulate smooth muscle cell differentiation.Arteriosclerosis, thrombosis, and vascular biology · 2011Review
- A phospholipase Cγ1-activated pathway regulates transcription in human vascular smooth muscle cells.Cardiovascular research · 2011Article
- cGMP-dependent protein kinase and the regulation of vascular smooth muscle cell gene expression: possible involvement of Elk-1 sumoylation.American journal of physiology. Heart and circulatory physiology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Understanding the mechanism of smooth muscle cell (SMC) differentiation will provide the foundation for elucidating SMC-related diseases, such as atherosclerosis, restenosis, and asthma. In the current study, overexpression of Elk-1 in SMCs down-regulated expression of several endogenous smooth muscle-restricted proteins, including telokin, SM22alpha, and smooth muscle alpha-actin. In contrast, down-regulation of endogenous Elk-1 in smooth muscle cells increased the expression of only telokin and SM22alpha, suggesting that smooth muscle-specific promoters are differentially sensitive to the inhibitory effects of Elk-1. Consistent with this, overexpression of the DNA binding domain of Elk-1, which acts as a dominant-negative protein by displacing endogenous Elk-1, enhanced the expression of telokin and SM22alpha without affecting expression of smooth muscle alpha-actin. Elk-1 suppressed the activity of smooth muscle-restricted promoters, including the telokin promoter that does not contain a consensus Elk-1 binding site, through its ability to block myocardin-induced activation of the promoters. Gel mobility shift and chromatin immunoprecipitation assays revealed that Elk-1 binds to a nonconsensus binding site in the telokin promoter and Elk-1 binding is dependent on serum response factor (SRF) binding to a nearby CArG box. Although overexpression of the SRF-binding B-box domain of Elk-1 is sufficient to repress the myocardin activation of the telokin promoter, this repression is not as complete as that seen with an Elk-1 fragment that includes the DNA binding domain. In addition, reporter gene assays demonstrate that an intact Elk-1 binding site in the telokin promoter is required for Elk-1 to maximally inhibit promoter activity. Together, these data suggest that the differential sensitivity of smooth muscle-specific genes to inhibition by Elk-1 may play a role in the complex changes in smooth muscle-specific protein expression that are observed under pathological conditions.
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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.