ArticleThe Journal of clinical investigation2005
5' CArG degeneracy in smooth muscle alpha-actin is required for injury-induced gene suppression in vivo.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 101 citations in OpenAlex.
- Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026Review
- Defective vascular smooth muscle cell tafazzin impairs mitochondrial function and promotes atherosclerosis in preclinical models.Nature communications · 2025Article
- Synergistic effects of micropatterned substrates and transforming growth factor-β1 on differentiation of human mesenchymal stem cells into vascular smooth muscle cells through modulation of Krϋppel-like factor 4.In vitro cellular & developmental biology. Animal · 2025Article
- Methamphetamine induces thoracic aortic aneurysm/dissection through C/EBPβ.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- H3K4 di-methylation governs smooth muscle lineage identity and promotes vascular homeostasis by restraining plasticity.Developmental cell · 2021Article
- Purine-rich element binding protein B attenuates the coactivator function of myocardin by a novel molecular mechanism of smooth muscle gene repression.Molecular and cellular biochemistry · 2021Article
- Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury.Communications biology · 2021Article
- Serum response factor-cofactor interactions and their implications in disease.The FEBS journal · 2021Review
- SIRT6 Protects Smooth Muscle Cells From Senescence and Reduces Atherosclerosis.Circulation research · 2021Article
- Adapter Protein RapGEF1 Is Required for ERK1/2 Signaling in Response to Elevated Phosphate in Vascular Smooth Muscle Cells.Journal of vascular research · 2021Article
- MicroRNA26 attenuates vascular smooth muscle maturation via endothelial BMP signalling.PLoS genetics · 2019Article
- Upregulation of the actin cytoskeleton via myocardin leads to increased expression of type 1 collagen.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Differentiated Smooth Muscle Cells Generate a Subpopulation of Resident Vascular Progenitor Cells in the Adventitia Regulated by Klf4.Circulation research · 2017Article
- Set7 mediated interactions regulate transcriptional networks in embryonic stem cells.Nucleic acids research · 2016Article
- A New Editor of Smooth Muscle Phenotype.Circulation research · 2016Article
- Nuclear PTEN functions as an essential regulator of SRF-dependent transcription to control smooth muscle differentiation.Nature communications · 2016Article
- Myocardin regulates vascular smooth muscle cell inflammatory activation and disease.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Myocardin in biology and disease.Journal of biomedical research · 2015Review
- Modulation of cysteine-rich protein 2 expression in vascular injury and atherosclerosis.Molecular biology reports · 2014Article
- Extracellular matrix synthesis in vascular disease: hypertension, and atherosclerosis.Journal of biomedical research · 2014Review
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6 authors at 1 institution in 1 country.
Funding
Abstract
CC(A/T)6GG-dependent (CArG-dependent) and serum response factor-dependent (SRF-dependent) mechanisms are required for gene expression in smooth muscle cells (SMCs). However, an unusual feature of many SMC-selective promoter CArG elements is that they contain a conserved single G or C substitution in their central A/T-rich region, which reduces binding affinity for ubiquitously expressed SRF. We hypothesized that this CArG degeneracy contributes to cell-specific expression of smooth muscle alpha-actin in vivo, since substitution of c-fos consensus CArGs for the degenerate CArGs resulted in relaxed specificity in cultured cells. Surprisingly, our present results show that these substitutions have no effect on smooth muscle-specific transgene expression during normal development and maturation in transgenic mice. However, these substitutions significantly attenuated injury-induced downregulation of the mutant transgene under conditions where SRF expression was increased but expression of myocardin, a smooth muscle-selective SRF coactivator, was decreased. Finally, chromatin immunoprecipitation analyses, together with cell culture studies, suggested that myocardin selectively enhanced SRF binding to degenerate versus consensus CArG elements. Our results indicate that reductions in myocardin expression and the degeneracy of CArG elements within smooth muscle promoters play a key role in phenotypic switching of smooth muscle cells in vivo, as well as in mediating responses of CArG-dependent smooth muscle genes and growth regulatory genes under conditions in which these 2 classes of genes are differentially expressed.
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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.