ArticleCirculation research2013
Smad2 and myocardin-related transcription factor B cooperatively regulate vascular smooth muscle differentiation from neural crest cells.
Article in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- Preclinical modeling of Loeys-Dietz syndrome: insights into mechanisms and therapy.Orphanet journal of rare diseases · 2026Review
- ELMO2 is an essential regulator of carotid artery development.Nature communications · 2025Article
- Generation of a novel constitutive smooth muscle cell-specific Myh11-driven Cre mouse model.Journal of molecular and cellular cardiology · 2025Article
- TGFBR3 dependent mechanism of TGFB2 in smooth muscle cell differentiation and implications for TGFB2-related aortic aneurysm.Stem cells translational medicine · 2025Article
- Greater TIMP-1 protein levels and neointimal formation represent sex-dependent cellular events limiting aortic vessel expansion in female rats.IUBMB life · 2024Article
- SMAD4: A critical regulator of cardiac neural crest cell fate and vascular smooth muscle development.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Article
- Smooth Muscle Heterogeneity and Plasticity in Health and Aortic Aneurysmal Disease.International journal of molecular sciences · 2023Review
- Smurf2-induced degradation of SMAD2 causes inhibition of hair follicle stem cell differentiation.Cell death discovery · 2022Article
- Association of TGF-β Canonical Signaling-Related Core Genes With Aortic Aneurysms and Aortic Dissections.Frontiers in pharmacology · 2022Review
- hiPSC Modeling of Lineage-Specific Smooth Muscle Cell Defects Caused byCirculation · 2021Article
- Sca1Stem cell reviews and reports · 2021Article
- Generation of Vascular Smooth Muscle Cells From Induced Pluripotent Stem Cells: Methods, Applications, and Considerations.Circulation research · 2021Review
- Surfactant Protein A, a Novel Regulator for Smooth Muscle Phenotypic Modulation and Vascular Remodeling-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- In Vitro Lineage-Specific Differentiation of Vascular Smooth Muscle Cells in Response to SMAD3 Deficiency: Implications for SMAD3-Related Thoracic Aortic Aneurysm.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Vascular smooth muscle cells in atherosclerosis.Nature reviews. Cardiology · 2019Review
- Long non-coding RNA SNHG16 regulates human aortic smooth muscle cell proliferation and migration via sponging miR-205 and modulating Smad2.Journal of cellular and molecular medicine · 2019Article
- Modeling elastin-associated vasculopathy with patient induced pluripotent stem cells and tissue engineering.Cellular and molecular life sciences : CMLS · 2019Review
- Glycoprotein M6B Interacts with TβRI to Activate TGF-β-Smad2/3 Signaling and Promote Smooth Muscle Cell Differentiation.Stem cells (Dayton, Ohio) · 2019Article
- Lineage-specific events underlie aortic root aneurysm pathogenesis in Loeys-Dietz syndrome.The Journal of clinical investigation · 2019Article
- Response Gene to Complement 32 Maintains Blood Pressure Homeostasis by Regulating α-Adrenergic Receptor Expression.Circulation research · 2018Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
rationaleVascular smooth muscle cell (VSMC) differentiation from neural crest cells (NCCs) is critical for cardiovascular development, but the mechanisms remain largely unknown.
objectiveTransforming growth factor-β (TGF-β) function in VSMC differentiation from NCCs is controversial. Therefore, we determined the role and mechanism of a TGF-β downstream signaling intermediate Smad2 in NCC differentiation to VSMCs. METHODS AND
resultsBy using Cre/loxP system, we generated a NCC tissue-specific Smad2 knockout mouse model and found that Smad2 deletion resulted in defective NCC differentiation to VSMCs in aortic arch arteries during embryonic development and caused vessel wall abnormality in adult carotid arteries where the VSMCs are derived from NCCs. The abnormalities included 1 layer of VSMCs missing in the media of the arteries with distorted and thinner elastic lamina, leading to a thinner vessel wall compared with wild-type vessel. Mechanistically, Smad2 interacted with myocardin-related transcription factor B (MRTFB) to regulate VSMC marker gene expression. Smad2 was required for TGF-β-induced MRTFB nuclear translocation, whereas MRTFB enhanced Smad2 binding to VSMC marker promoter. Furthermore, we found that Smad2, but not Smad3, was a progenitor-specific transcription factor mediating TGF-β-induced VSMC differentiation from NCCs. Smad2 also seemed to be involved in determining the physiological differences between NCC-derived and mesoderm-derived VSMCs.
conclusionsSmad2 is an important factor in regulating progenitor-specific VSMC development and physiological differences between NCC-derived and mesoderm-derived VSMCs.
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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.