OBJECTIVE:
Dermal papilla cells are required for inducing epithelial stem cells during hair morphogenesis and regeneration. Adult human dermal papilla cells lose their hair inductive capacity after several in vitro culture passages. Maintaining the hair-inductive capacity of adult human dermal papilla cells is an obstacle that needs to be overcome in order to realize tissue engineered hair follicles. We hypothesized that connective tissue growth factor (CTGF), a fibrogenic factor known to influence Wnt, BMP, and TGF-β could influence key signaling pathways in human dermal papilla cells. The purpose of this study was to determine the effect of exogenous connective tissue growth factor on cultured human dermal papilla cells.
METHODS:
Adult human dermal papilla cells were isolated and cultured in the presence of CTGF (20ng/ml or 40ng/ml). Human dermal papilla cells positivity was determined using the alkaline phosphatase immunofluorescence. After treatment with CTGF, the proliferation of human dermal papilla cells was assessed. The presence of connective tissue growth factor in human dermal papilla cells was identified by immunofluorescence. The α-smooth muscle actin protein expression was evaluated by western blot. Gene expression profile of Wnt, BMP, TGF-β signaling pathways and alkaline phosphatase, versican activity, were determined using real time RT-PCR.
RESULTS:
CTGF reduced proliferation rate of cultured human dermal papilla cells in a dose-dependent manner. Exogenous connective tissue growth factor increased the expression of cytoplasmic connective tissue growth factor, and increased mRNA expression of alkaline phosphatase and β-catenin, BMP2 and TGF-β2 in human dermal papilla cells. Versican mRNA level was suppressed and a small increase in α-smooth muscle actin protein expression was observed.
CONCLUSION:
Exogenous connective tissue growth factor can preserve the innate hair-inductive ability of adult human dermal papilla cells in vitro cultures, which is controlled through the Wnt, BMP and TGF-β signaling pathways. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
