Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.] · 2008
Expression of Smad protein by normal skin fibroblasts and hypertrophic scar fibroblasts in response to transforming growth factor beta1.
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Xie Ju-lin, Qi Shao-hai, Pan Shu, Xu Ying-bin, Li Tian-zeng, Liu Xu-sheng, Liu Po
Аннотация
BACKGROUND: Smad proteins are important intracellular mediators of transforming growth factor (TGF)-beta signaling. Little has been known about the specific relationship between TGF-beta and TGF-beta/Smad signaling in hypertrophic scars.
OBJECTIVE: The objective was to investigate the expression of Smads and the specific relationship between TGF-beta and TGF-beta/Smad signaling in hypertrophic scars.
METHODS: In this study, we initially determined the endogenous protein levels of Smad2 and Smad7 in hypertrophic scar fibroblast (HSFs) and normal skin fibroblast (NSFs). Second, we stimulated HSFs and NSFs with recombinant human TGF-beta1 for 24 hours to determine whether the TGF-beta1 could potentiate its effect by further stimulating the production of Smad by reverse transcription-polymerase chain reaction and Western blot analysis.
RESULTS: When compared with NSFs, the endogenous expression of Smad2 in HSFs was up-regulated and TGF-beta1 could further stimulate the production of Smad2. Although the levels of Smad7 were similar between HSFs and NSFs, TGF-beta1 up-regulated the expression of Smad7 for NSFs only, with no discernible effect on HSFs. These changes were paralleled by a significant increase in cytoplasm-to-nuclear translocation of Smad2.
CONCLUSION: These data substantiated the model of an autocrine positive loop in hypertrophic scars pathogenesis. The authors have indicated no significant interest with commercial supporters.
OBJECTIVE: The objective was to investigate the expression of Smads and the specific relationship between TGF-beta and TGF-beta/Smad signaling in hypertrophic scars.
METHODS: In this study, we initially determined the endogenous protein levels of Smad2 and Smad7 in hypertrophic scar fibroblast (HSFs) and normal skin fibroblast (NSFs). Second, we stimulated HSFs and NSFs with recombinant human TGF-beta1 for 24 hours to determine whether the TGF-beta1 could potentiate its effect by further stimulating the production of Smad by reverse transcription-polymerase chain reaction and Western blot analysis.
RESULTS: When compared with NSFs, the endogenous expression of Smad2 in HSFs was up-regulated and TGF-beta1 could further stimulate the production of Smad2. Although the levels of Smad7 were similar between HSFs and NSFs, TGF-beta1 up-regulated the expression of Smad7 for NSFs only, with no discernible effect on HSFs. These changes were paralleled by a significant increase in cytoplasm-to-nuclear translocation of Smad2.
CONCLUSION: These data substantiated the model of an autocrine positive loop in hypertrophic scars pathogenesis. The authors have indicated no significant interest with commercial supporters.