ArticleThe Journal of biological chemistry2011
Smad3-mediated myocardin silencing: a novel mechanism governing the initiation of smooth muscle differentiation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Myeloid Ecotropic Viral Integration Site 1 Promotes Vascular Smooth Muscle Differentiation through Activation of Myocardin.bioRxiv : the preprint server for biology · 2026Article
- BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells.International journal of molecular sciences · 2025Article
- Surfactant Protein A, a Novel Regulator for Smooth Muscle Phenotypic Modulation and Vascular Remodeling-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- LncRNA GAS5 attenuates fibroblast activation through inhibiting Smad3 signaling.American journal of physiology. Cell physiology · 2020Article
- Article
- Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk.PLoS genetics · 2018Article
- Mesenchyme homeobox 1 mediates transforming growth factor-β (TGF-β)-induced smooth muscle cell differentiation from mouse mesenchymal progenitors.The Journal of biological chemistry · 2018Article
- Opposing Actions of AKT (Protein Kinase B) Isoforms in Vascular Smooth Muscle Injury and Therapeutic Response.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Curcumin enhances vascular contractility via induction of myocardin in mouse smooth muscle cells.Acta pharmacologica Sinica · 2017Article
- Olfactomedin 2 Regulates Smooth Muscle Phenotypic Modulation and Vascular Remodeling Through Mediating Runt-Related Transcription Factor 2 Binding to Serum Response Factor.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Yes-Associated Protein Inhibits Transcription of Myocardin and Attenuates Differentiation of Vascular Smooth Muscle Cell from Cardiovascular Progenitor Cell Lineage.Stem cells (Dayton, Ohio) · 2017Article
- TGF-β/SMAD3 Pathway Stimulates Sphingosine-1 Phosphate Receptor 3 Expression: IMPLICATION OF SPHINGOSINE-1 PHOSPHATE RECEPTOR 3 IN LUNG ADENOCARCINOMA PROGRESSION.The Journal of biological chemistry · 2016Article
- Smooth Muscle Cell Proangiogenic Phenotype Induced by Cyclopentenyl Cytosine Promotes Endothelial Cell Proliferation and Migration.The Journal of biological chemistry · 2016Article
- Aberrant Expression of microRNA-9 Contributes to Development of Intracranial Aneurysm by Suppressing Proliferation and Reducing Contractility of Smooth Muscle Cells.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Transforming growth factor β1 antagonizes the transcription, expression and vascular signaling of guanylyl cyclase/natriuretic peptide receptor A - role of δEF1.The FEBS journal · 2016Article
- Transcriptional profiling reveals crosstalk between mesenchymal stem cells and endothelial cells promoting prevascularization by reciprocal mechanisms.Stem cells and development · 2015Article
- Myocardin in biology and disease.Journal of biomedical research · 2015Review
- The magic touch: endothelial cells muscle-up adipose.Circulation research · 2014Article
- Generation of a Cre knock-in into the Myocardin locus to mark early cardiac and smooth muscle cell lineages.Genesis (New York, N.Y. : 2000) · 2014Article
- Cell division cycle 7 mediates transforming growth factor-β-induced smooth muscle maturation through activation of myocardin gene transcription.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Both TGF-β and myocardin (MYOCD) are important for smooth muscle cell (SMC) differentiation, but their precise role in regulating the initiation of SMC development is less clear. In TGF-β-induced SMC differentiation of pluripotent C3H10T1/2 progenitors, we found that TGF-β did not significantly induce Myocd mRNA expression until 18 h of stimulation. On the other hand, early SMC markers such as SM α-actin, SM22α, and SM calponin were detectable beginning 2 or 4 h after TGF-β treatment. These results suggest that Myocd expression is blocked during the initiation of TGF-β-induced SMC differentiation. Consistent with its endogenous expression, Myocd promoter activity was not elevated until 18 h following TGF-β stimulation. Surprisingly, Smad signaling was inhibitory to Myocd expression because blockade of Smad signaling enhanced Myocd promoter activity. Overexpression of Smad3, but not Smad2, inhibited Myocd promoter activity. Conversely, shRNA knockdown of Smad3 allowed TGF-β to activate the Myocd promoter in the initial phase of induction. Myocd was activated by PI3 kinase signaling and its downstream target Nkx2.5. Interestingly, Smad3 did not affect PI3 kinase activity. However, Smad3 physically interacted with Nkx2.5. This interaction blocked Nkx2.5 binding to the Myocd promoter in the early stage of TGF-β induction, leading to inhibition of Myocd mRNA expression. Moreover, Smad3 inhibited Nkx2.5-activated Myocd promoter activity in a dose-dependent manner. Taken together, our results reveal a novel mechanism for Smad3-mediated inhibition of Myocd in the initiation phase of SMC differentiation.
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Registered trials
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.