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TGFβ1-induced Baf60c regulates both smooth muscle cell commitment and quiescence
Abhishek Sohni1, Francesca Mulas, Fulvia Ferrazzi
1Stem Cell Institute, Department of Development and Regeneration, K.U.Leuven, Leuven, Belgium.
Plos One
|October 31, 2012
Summary
Transforming growth factor beta 1 (TGFβ1) signaling induces smooth muscle cell (SMC) differentiation from rat multipotent adult progenitor cells (rMAPCs). BAF60c acts as a key co-regulator in this TGFβ1-mediated process, influencing SMC gene expression and phenotype.
Area of Science:
- Stem cell biology
- Molecular and cell biology
- Developmental biology
Background:
- Smooth muscle cells (SMCs) are crucial in disease, but their developmental mechanisms are not fully understood.
- Transforming growth factor beta 1 (TGFβ1) signaling is established to influence SMC development, yet downstream molecular regulators require further elucidation.
Purpose of the Study:
- To investigate the molecular mechanisms underlying smooth muscle cell differentiation from multipotent adult progenitor cells (MAPCs).
- To identify downstream molecular signals of TGFβ1 that regulate SMC development.
Main Methods:
- Utilized rat multipotent adult progenitor cell (rMAPC) lines for differentiation studies.
- Performed genome-wide transcriptome analysis to identify key regulatory genes.
- Employed gene knockdown and ectopic expression to assess the function of BAF60c.
- Conducted chromatin- and co-immunoprecipitation assays to determine molecular interactions.
Main Results:
- TGFβ1, with or without PDGF-BB, induced rMAPC differentiation into SMCs expressing key structural proteins like αSMA.
- BAF60c (SMARCD3/BAF60c), a component of the SWI/SNF chromatin remodeling complex, was significantly upregulated during MAPC-SMC differentiation.
- BAF60c was identified as a necessary co-regulator for TGFβ1-induced SMC gene expression, with knockdown decreasing and ectopic expression promoting SMC commitment.
- TGFβ1 activates BAF60c via SMAD2/3 binding to its promoter, and BAF60c regulates SMC genes through interaction with SRF at CArG box elements.
- BAF60c overexpression led to an immature SMC phenotype, characterized by increased proliferation and reduced contractile marker expression.
Conclusions:
- BAF60c is essential for TGFβ1-mediated commitment of rMAPCs to SMCs.
- BAF60c is implicated in inducing a proliferative state in quiescent SMCs.
- The MAPC-SMC differentiation model offers a valuable platform for discovering additional regulators of SMC development.
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