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Cross‐Talk between CTGF and TGF‐β1 in Mesenchymal Stem Cell (MSC) Condensation
Author(s) -
CarpioCano Fabiola Del,
Belcher Joyce,
Buck Kimberly B,
Popoff Steven N,
Cadena Raul A DeLa,
Safadi Fayez F
Publication year - 2007
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.21.5.a229-c
Subject(s) - ctgf , chemistry , mesenchymal stem cell , microbiology and biotechnology , transforming growth factor , growth factor , biology , biochemistry , receptor
The aggregation of MSC is critical for chondrocyte differentiation. TGF‐β1 acts to promote MSC condensation, proliferation and differentiation. Connective tissue growth factor (CTGF) is matricellular protein expressed in MSC condensation and regulates matrix production and differentiation. Previous studies showed that CTGF acts downstream mediator of TGF‐β1‐induced MSC condensation and silencing of CTGF expression inhibits MSC condensation induced by TGF‐β1. Here we examined the crosstalk between CTGF and TGF‐β1 to stimulate MSC condensation. We assessed MSC condensation induced by TGF‐β1 using C3H10T1/2 cells infected with either adenovirus expressing GFP (control) or GFP‐CTGF. CTGF overexpression inhibited TGF‐β1‐induced MSC condensation when compared to controls. These data suggest that CTGF expression is tightly regulated during MSC condensation. Next, we examined the MAP Kinase family to elucidate the inhibitory effect of CTGF on MSC condensation induced by TGF‐β1. Phosphorylated P38, Junk and Erk were increased in the GFP infected MCS treated with TGF‐β1. However, MSC infected with GFP‐CTGF and treated with TGF‐β1 showed only an increase in phosphorylated Jnk and Erk but not P38. These findings indicate that p38 MAPK may mediate MSC condensation by TGF‐β1. Further studies are warranted to elucidate the role of P38 in mediating CTGF/TGF‐β1 effects on MSC condensation.