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

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

PROVIDER: PRJNA843675 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19445719.fastq.gz	Fastqsanger.gz
	SRR19445720.fastq.gz	Fastqsanger.gz
	SRR19445721.fastq.gz	Fastqsanger.gz
	SRR19445722.fastq.gz	Fastqsanger.gz

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

Project description: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.

2023-07-01 | GSE205075 | GEO

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.

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Microarray expression profile analysis of long non-coding RNA in androgenetic alopecia: a study of Chinese men

Project description:To examined the genome-wide expression levels of lncRNAs in androgenetic alopecia tissues and paired adjacent normal tissues by microarray analysis. We identified numerous lncRNAs that were differentially regulated between androgenetic alopecia and paired normal tissues.

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Protein Profiling of Forehead and Scalp Corneocytes in Androgenetic versus Frontal Fibrosing Alopecia

Project description:Protein profiling offers an effective approach to characterizing the departure from normal of epidermis in disease states. The present investigation tested the hypothesis that the differentiation of epidermal corneocytes is perturbed in the forehead of subjects exhibiting frontal fibrosing alopecia. To this end, samples were collected by tape stripping from subjects diagnosed with this condition and compared to those from asymptomatic control subjects and from those exhibiting androgenetic alopecia. Unlike the latter, which exhibited only 3 proteins significantly different from controls, forehead samples from frontal fibrosing alopecia subjects displayed 72 proteins significantly different from controls, nearly two-thirds having lower expression. Comparison to corresponding profiles in scalp samples from frontal fibrosing alopecia and androgenetic alopecia suggested the perturbation of epidermal differentiation in the former was even greater in the scalp.

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Spatial transcriptome reveals disturbance of peri-infundibular immune infiltration in androgenetic alopecia

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Adipose transcriptome in the scalp of androgenetic alopecia

Project description:Adipose transcriptome in the scalp of androgenetic alopecia

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Project description:Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (AGA); yet the mechanisms for decreased hair growth in this disorder are unclear. Here, we show that prostaglandin D2 synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D2 (PGD2), is similarly elevated in bald scalp. During normal follicle cycling in mice Ptgds and PGD2 levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD2 inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD2 receptor G protein-coupled receptor 44 (GPR44), but not the prostaglandin D2 receptor 1(PTGDR). Furthermore, we find that a transgenic mouse, K14-Ptgs2, which targets prostaglandin-endoperoxide synthase 2 expression to the skin, demonstrates elevated levels of PGD2 in the skin and develops alopecia, follicular miniaturization and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD2 as an inhibitor of hair growth in AGA and suggest the PGD2-GPR44 pathway as a potential target for treatment. 5 individuals with Androgenetic Alopecia were biopsied at both their haired and bald scalp for mRNA purification and microarray (total 10 arrays)

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Spatial transcriptome reveals disturbance of peri-infundibular immune infiltration in androgenetic alopecia

Project description:Spatial transcriptome reveals disturbance of peri-infundibular immune infiltration in androgenetic alopecia

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