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Journal of the Korean Society for Aesthetic Plastic Surgery 2005;11(2):229-236.
Published online September 1, 2005.
The Effects of Anti-keloid Drugs on the Expressions of Fibronectin, Transforming Growth Factor-beta and Transforming Growth Factor-beta Receptor in Keloid Fibroblast.
Jung Min Park, Min Hyuk Lee, Keun Cheol Lee, Seok Kwun Kim, Hae Rhan Bae, Seo Hee Rha
1Department of Plastic & Reconstructive Surgery, College of Medicine, Dong-A University, Busan, Korea. jmpark@daunet.donga.ac.kr
2Department of Physiology, College of Medicine, Dong-A University, Busan, Korea.
3Department of Anatomical Pathology, College of Medicine, Dong-A University, Busan, Korea.
Abstract
Keloids represent a dysregulated response to cutaneous wounding that results in an excessive deposition of extracellular matrix. However, the molecular mechanisms underlying this pathologic deposition of extracellular matrix still remain to be elucidated. In this study, the effects of anti-keloid drugs (triamcinolone(R), 5-FU(R), bleomycin(R), verapamil(R)) on the expression of fibronectin and TGF-beta and its receptor in keloid fibroblasts were evaluated in vitro. Human keloid fibroblasts(KFs) and normal human dermal fibroblasts(NHDFs) were isolated from earlobe keloids. Immunoprecipitation and Western blot of fibronectin, ELISA of TGF-beta secretion and Western blot of TGF-beta receptor were performed using the primary cultured fibroblasts treated with various drugs. TGF-beta secretion was increased in keloid fibroblasts compared to NHDFs. TGF-beta promoted fibronectin synthesis in keloid fibroblasts. These results substantiate the hypothesis that the elevated levels of TGF-beta play a potential role in keloid pathogenesis. 5-FU suppressed profoundly TGF-beta secretion. Triamcinolone and verapamil inhibited significantly fibronectin synthesis and secretion, and also suppressed TGF-beta receptor expression in keloid fibroblasts. In conclusion, it is postulated that the combination of low dose of 5-FU and triamcinolone or verapamil may be useful in keloid treatment by the additive effect of different anti-keloid action.
Key Words: Keloid, Fibroblasts, Fibronectins, TGF-beta, TGF-beta recepter
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