Perifollicular fibrosis: Pathogenetic role in androgenetic alopecia

Abstract

Androgenetic 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: 10-9-10-7M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10-8M) 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-β1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-β1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-β1 antibody (10 μg/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-β1 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-β1 expression may explain another possible mechanism how finasteride works in AGA. © 2006 Pharmaceutical Society of Japan.