Perifollicular fibrosis: pathogenetic role in androgenetic alopecia
Autor: | Jin Ho Chung, Hyun Keol Pyo, Kyu Han Kim, Oh Sang Kwon, Jin Sook Kim, Hyeon Gyeong Yoo, Hee Chul Eun, S R Lee, Kwang Hyun Cho, Jong Hee Lee, Hyung In Moon |
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Rok vydání: | 2006 |
Předmět: |
medicine.medical_specialty
medicine.drug_class Blotting Western Cell Culture Techniques Pharmaceutical Science Enzyme-Linked Immunosorbent Assay Biology Collagen Type I Transforming Growth Factor beta1 chemistry.chemical_compound Fibrosis Internal medicine Follicular phase medicine Humans Testosterone RNA Messenger Cells Cultured Pharmacology Messenger RNA integumentary system Reverse Transcriptase Polymerase Chain Reaction Finasteride Antibodies Monoclonal Alopecia General Medicine Fibroblasts medicine.disease Androgen Procollagen peptidase Endocrinology chemistry Dihydrotestosterone Hair Follicle medicine.drug |
Zdroj: | Biologicalpharmaceutical bulletin. 29(6) |
ISSN: | 1347-5215 |
Popis: | 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(-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. |
Databáze: | OpenAIRE |
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