Premium
α‐Smooth muscle actin differential regulation in hESC derived mesenchymal cells
Author(s) -
Boyd Nolan Lee,
Stice Steven L.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1030.2
Subject(s) - mesenchymal stem cell , cd90 , microbiology and biotechnology , chemistry , cd34 , progenitor cell , biology , stem cell
We have derived mesenchymal cell lines from H9 hESC in a monolayer culture. The derived cells are positive for multiple mesenchymal markers (CD73, CD90, CD105 and CD166) while being negative for markers of hematopoietic and endothelial precursors (CD31, CD34, CD45, CD133 and CD146). Seeding the cells into a collagen I lattice (24‐well plate, 1ml of rat tail collagen I [1mg/ml] and 1.25x10 5 cells/ml) for 7d demonstrated they are highly contractile reducing the construct to ~25% of its original size. We have also demonstrated the derived cells can differentiate toward osteogenic and chondrogenic cells, but not adipogenic suggesting they are a mesenchymal progenitor cell. It is suggested that MSC are capable of also differentiating into smooth muscle cells (SMC), therefore we examined their ability to express αSMA when exposed to various growth factors (TGF‐β1 and PDGF‐B) and serum. Cells grown in serum‐free media showed varying amounts of αSMA by Western blot, but when exposed to TGFβ1 (1 ng/ml) there was a consistent up‐regulation of αSMA protein. In contrast, both PDGF‐B (10 ng/ml) and serum (10%) did not produce any expression of αSMA. This suggests the derived mesenchymal cells may have differential regulation of αSMA expression and could be a model for SMC differentiation from precursor cells. This research was supported by grants and fellowships from NIH and GTEC.