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RNA-microarray analyses and protein profiles from affected and clinically non-affected scalp in male androgenetic alopecia patients

ABSTRACT: The aim of this pilot study was to combine standard clinical diagnostics with RNA and protein analyses from non-invasively obtained material. In 6 male volunteers with AGA, Norwood-Hamilton stage IIIv-IV, we performed global photography, phototrichogram, pH and sebum measurements, as well as skin surface cytokine measurements on AGA-affected frontal and vertex scalp skin compared to clinically unaffected occiput.

ORGANISM(S): Homo sapiens

PROVIDER: GSE78722 | GEO | 2017/06/30

SECONDARY ACCESSION(S): PRJNA313322

REPOSITORIES: GEO

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Study of gene expression alteration in male androgenetic alopecia: evidence of predominant molecular signaling pathways

Project description:Background: The male androgenetic alopecia (AGA) is the most common form of hair loss in men and is hereditary in more than 80% of cases and characterized by a distinct pattern of progressive hair loss starting from the frontal area and the vertex of the scalp. Although several genetic risk loci have been identified, relevant genes for AGA remain to be identified. Objectives: Herein, molecular biomarkers associated with premature AGA were identified through gene expression analysis using cDNA generated from scalp skin vertex biopsies of hairless/bold men with premature AGA and healthy volunteers. Results: This monocentric study reveals that genes encoding mast cell granule enzymes, inflammatory and immunoglobulin-associated immune mediators were significantly over-expressed in AGA. In contrast, under-expressed genes appear to be associated with the Wnt/β-catenin and BMP/TGF-β signaling pathways. Although the involvement of these pathways in hair follicle regeneration is well-described, functional interpretation of the transcriptomic data highlights different events that account for their inhibition. In particular, one of these events depends on the dysregulated expression of proopiomelanocortin (POMC), as confirmed by RT-qPCR and immunohistochemistry. In addition, a lower expression of CYP27B1 in AGA patients supports that alteration of vitamin D metabolism contributes to hair loss. Conclusion: Altogether, this study provides evidence for distinct molecular events contributing to alopecia that might be targeted for new therapeutic approaches.

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Prostaglandin D2 Inhibits Hair Growth and Is Elevated in Bald Scalp of Men with Androgenetic Alopecia

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)

2012-03-26 | E-GEOD-36169 | biostudies-arrayexpress

Prostaglandin D2 Inhibits Hair Growth and Is Elevated in Bald Scalp of Men with Androgenetic Alopecia

2012-03-26 | GSE36169 | GEO

RNA-Seq of anagen pilosebaceous units (PUs) isolated from occipital and vertex scalp regions of 10 Hamilton grade IV male androgenetic alopecia (AGA) volunteers

Project description:RNA-Seq of anagen pilosebaceous units (PUs) isolated from occipital and vertex scalp regions of 10 Hamilton grade IV male androgenetic alopecia (AGA) volunteers

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A novel Long non-coding RNA AL136131.3 inhibits hair growth through mediating glycolysis in androgen alopecia

Project description:The key pathophysiological changes in androgenetic alopecia (AGA) are limited to hair follicles (HFs) in frontal and vertex regions, except for the occipital region. To identify biological differences among HF subpopulations. Paired vertex and occipital HFs from 10 male AGA donors were collected for RNA-seq assay. Furthermore, hair follicle and cell experiments were conducted on the identified key genes to reveal their roles in AGA. Our study aimed to uncover potential lncRNA indicators for AGA and reveal the potential mechanism underlying the involvement of AL136131.3 in hair growth in AGA.

2022-09-02 | GSE212301 | GEO

RNA-Seq of anagen pilosebaceous units (PUs) isolated from occipital and vertex scalp regions of 10 Hamilton grade IV male androgenetic alopecia (AGA) volunteers

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2020-11-30 | E-MTAB-9557 | biostudies-arrayexpress

Transcripotome analysis of different locations of hair follicles (bulb, bulge) in androgenetic alopecia

Project description:To fully interrogate location-specific variations of the hair follicle in AGA and normal persons, we sought to perform a thorough and comprehensive transcripotome profiling of different locations of hair follicles (bulb portions, bulge portions) in balding and non-balding areas of AGA, with normal comparisons.

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Genome-wide association data on male-pattern baldness

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Bald scalp retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells

Project description:Androgenetic alopecia (AGA) or common baldness results from a marked decrease in hair follicle size. This miniaturization may be related to loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from the same individuals for the presence of hair follicle stem and progenitor cells using flow cytometry to quantitate cells expressing CYTOKERATIN 15 (KRT15), CD200, CD34 and ALPHA-6-INTEGRIN (ITGA6). High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. Cells with the highest level of KRT15 expression were maintained in bald scalp; however, distinct populations of CD200high ITGA6high cells and CD34-positive cells were markedly diminished. Consistent with a progenitor cell phenotype, the diminished populations localized closely to the stem-cell rich bulge area but were larger and more proliferative than the bulge stem cells. In functional assays, analogous CD200 high /Itga6 high cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings suggest that a defect in stem cell activation plays a role in the pathogenesis of AGA. This SuperSeries is composed of the SubSeries listed below.

2011-01-12 | GSE21569 | GEO

Adipose transcriptome in the scalp of androgenetic alopecia

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2023-08-30 | GSE212757 | GEO

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