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AR/miR-221/IGF-1 pathway mediates the pathogenesis of androgenetic alopecia

ABSTRACT: Our data showed that miR-221 had a profound effect on the biological function of dermal papilla cells (DPCs) and dermal sheath cells (DSCs) of hair follicle. Overexpression of miR-221 affected the MAPK signaling in DPCs, and PI3K/AKT signaling in DSCs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE205075 | GEO | 2023/07/01

REPOSITORIES: GEO

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The homing of exogenous hair follicle mesenchymal stem cells into hair follicle niches

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AR/miR-221/IGF-1 pathway mediates the pathogenesis of androgenetic alopecia

Project description:AR/miR-221/IGF-1 pathway mediates the pathogenesis of androgenetic alopecia

| PRJNA843675 | ENA

The AR/miR-221/IGF-1 pathway mediates the pathogenesis of androgenetic alopecia.

Project description: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.

| S-EPMC10367565 | biostudies-literature

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