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

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

PROVIDER: PRJEB40307 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4580760_1.fastq.gz	Fastqsanger.gz
	ERR4580760_2.fastq.gz	Fastqsanger.gz
	ERR4580770_1.fastq.gz	Fastqsanger.gz
	ERR4580770_2.fastq.gz	Fastqsanger.gz
	ERR4580780_1.fastq.gz	Fastqsanger.gz

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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:10 pilosebaceous units (PUs) at the anagen phase were isolated from each involved (balding; vertex) and non-involved (control; occipital) scalp region using the follicular unit extraction (FUE) technique.

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

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)

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

Project description: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.

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

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Project description:To identify differentially expressed genes in androgenetic alopecia specifically in the adipose, adipose tissue samples from affected male participants were collected through punch biopsy at two different sites: bald (frontal) and normal (occipital,as control) scalp. After removal of the epidermis, dermis and hair follicle, we isolated RNA from the remaining adipose layer of the bald and normal scalp then performed gene expression analysis on the RNA-seq data to compare the profiles of the bald and normal scalp.

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Adipose transcriptome in the scalp of androgenetic alopecia

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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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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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