Linked Life Data

16755026

Source:http://linkedlifedata.com/resource/pubmed/id/16755026

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pubmed-article:16755026pubmed:abstractTextAndrogenetic alopecia (AGA) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 microg/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the AGA, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in AGA.lld:pubmed
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pubmed-article:16755026pubmed:year2006lld:pubmed
pubmed-article:16755026pubmed:articleTitlePerifollicular fibrosis: pathogenetic role in androgenetic alopecia.lld:pubmed
pubmed-article:16755026pubmed:affiliationDepartment of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University, Seoul, Korea.lld:pubmed
pubmed-article:16755026pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16755026pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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