期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 19, 期 11, 页码 3307-3323出版社
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.80481
关键词
androgenetic alopecia; miR-221; androgen receptor; IGF-1; dihydrotestosterone
The study found that miR-221 significantly suppressed hair growth and proliferation in AGA patients. Mechanistic analysis revealed that AR directly promoted miR-221 transcription, leading to the inactivation of the MAPK pathway in DPCs and the PI3K/AKT pathway in DSCs. MiR-221 could serve as a novel biomarker and potential therapeutic target for treating AGA.
Androgenetic alopecia (AGA) affects more than half of the adult population worldwide and is primarily caused by the binding of dihydrotestosterone (DHT) to androgen receptors (AR). However, the mechanisms by which AR affects hair follicles remain unclear. In our study, we found that miR-221 significantly suppressed hair growth and the proliferation of dermal papilla cells (DPCs) and dermal sheath cells (DSCs) in AGA patients. Interestingly, miR-221 and AR were mainly co-located in the same part of the hair follicle. Mechanistic analysis revealed that AR directly promoted the transcription of miR-221, which in turn suppressed IGF-1 expression, leading to the inactivation of the MAPK pathway in DPCs and the PI3K/AKT pathway in DSCs. In AGA patients, miR-221 expression was positively correlated with AR expression and negatively correlated with IGF-1 expression. Our findings indicate that miR-221, as a direct target of AR, plays a crucial role in the pathogenesis of AGA, making it a novel biomarker and potential therapeutic target for treating AGA.
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