ArticleAmerican journal of physiology. Cell physiology2011
Smad2 and PEA3 cooperatively regulate transcription of response gene to complement 32 in TGF-β-induced smooth muscle cell differentiation of neural crest cells.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Smooth Muscle Heterogeneity and Plasticity in Health and Aortic Aneurysmal Disease.International journal of molecular sciences · 2023Review
- RGCC balances self-renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex.EMBO reports · 2021Article
- RGC-32 and diseases: the first 20 years.Immunologic research · 2019Review
- Renal proteomic analysis of RGC-32 knockout mice reveals the potential mechanism of RGC-32 in regulating cell cycle.American journal of translational research · 2018Article
- Exogenous transforming growth factor-β1 enhances smooth muscle differentiation in embryonic mouse jejunal explants.Journal of tissue engineering and regenerative medicine · 2018Article
- Response Gene to Complement 32 in Vascular Diseases.Frontiers in cardiovascular medicine · 2018Review
- Response gene to complement 32 regulates the G2/M phase checkpoint during renal tubular epithelial cell repair.Cellular & molecular biology letters · 2016Article
- Response gene to complement 32 (RGC-32) expression on M2-polarized and tumor-associated macrophages is M-CSF-dependent and enhanced by tumor-derived IL-4.Cellular & molecular immunology · 2015Article
- Smad2 and myocardin-related transcription factor B cooperatively regulate vascular smooth muscle differentiation from neural crest cells.Circulation research · 2013Article
- A novel in vitro model system for smooth muscle differentiation from human embryonic stem cell-derived mesenchymal cells.American journal of physiology. Cell physiology · 2013Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Response gene to complement 32 (RGC-32) is activated by transforming growth factor- β (TGF-β) and plays an important role in smooth muscle cell (SMC) differentiation from neural crest Monc-1 cells. The molecular mechanism governing TGF-β activation of RGC-32, however, remains to be determined. The present studies indicate that TGF-β regulates RGC-32 gene transcription. Sequence analysis revealed a Smad binding element (SBE) located in the region from -1344 to -1337 bp upstream of the transcription start site of RGC-32 gene. A polyomavirus enhancer activator (PEA3) binding site is adjacent to the SBE. Mutation at either SBE or PEA3 site significantly inhibited RGC-32 promoter activity. Mutations at both sites completely abolished TGF-β-induced promoter activity. Biochemically, TGF-β stimulated recruitment of Smad2, Smad4, and PEA3 to the RGC-32 promoter, as revealed by gel shift and chromatin immunoprecipitation analyses. Functionally, Smad2, but not Smad3, activated RGC-32 promoter. PEA3 appeared to enhance Smad2 activity. In agreement with their function, Smad2, but not Smad3, physically interacted with PEA3. In TGF-β-induced SMC differentiation of Monc-1 cells, knockdown of Smad2 by short hairpin RNA resulted in downregulation of RGC-32 and SMC marker genes. The downregulation of SMC markers, however, was rescued by exogenously introduced RGC-32. These results demonstrate that Smad2 regulation of RGC-32 transcription is essential for SMC differentiation from neural crest cells.
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