Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE90594 | GEO | 2017/12/13

SECONDARY ACCESSION(S): PRJNA355129

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

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

Transcriptome profiling of human plucked frontal and occipital hair follicles

Project description:Androgenetic alopecia (AGA) is characterized by a progressive and androgen-dependent loss of hair from the frontal and vertex regions of the scalp. Although large-scale genetic analyses have identified >300 genetic risk factors, the underlying causal genes and pathways, and their involvement in core pathophysiological mechanisms, remain unclear. In the present study, systematic profiling of differential mRNA and microRNA expression was performed in human hair follicle samples from frontal and occipital scalp regions. Taken together, the present data improve understanding of the genomic regions, genes, and pathways that are implicated in AGA pathobiology.

| EGAS00001002832 | EGA

Metabolomics Analysis of Frontal Fibrosing Alopecia

Project description:Scarring alopecia consists of a collection of disorders characterized by destruction of hair follicles, replacement with fibrous scar tissue, and irreversible hair loss. Alopecia affects men and women worldwide and can be a significant source of psychological stress and depression for affected individuals. The purpose of this study was to explore metabolic profiles in scalp tissue samples from normal control subjects (n=6) and in matched samples obtained from affected (n=12) and unaffected (n=12) areas of the scalp in patients with lymphocytic Frontal Fibrosing Alopecia (FFA). Frontal fibrosing alopecia results from destruction of hair follicles by an inflammatory lymphocytic infiltrate that is localized around the upper portion of the hair follicle.

2014-07-24 | ST000093 | MetabolomicsWorkbench

Mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+)

Project description:Mouse back skin was disassociated to single cells, sorted by cell surface markers and tested by microarrray To compare the gene expression of mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+) xx Bald scalp retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells 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. 4 independent biologic replicates (each pooled from 3 distinct mice) were sorted for Mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+)

2011-01-12 | E-GEOD-21568 | biostudies-arrayexpress

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

Extensive alopecia areata is reversed by IL-23 cytokine antagonism

Project description:Alopecia areata (AA) is a prevalent disease associated with major emotional distress, and lacks effective, safe therapeutics for patients with extensive hair loss. This is the first report of hair regrowth with specific cytokine antagonism, in three patients with extensive hair loss ranging from 40% scalp involvement to alopecia universalis. Ustekinumab, an IL-12/23p40 antagonist that is highly effective in psoriasis, showed impressive ability to induce hair regrowth, coupled with suppression of inflammatory pathways and upregulation of hair keratins. Our report suggests that extensive AA is reversible using targeted treatments, opening the door for specific cytokine antagonism for this debilitating disease. We evaluated hair regrowth in three AA patients at 20 weeks after treatment with 3 subcutaneous doses of 90mg ustekinumab given at weeks 0, 4, and 16. Skin biopsies of lesional and non-lesional scalp (when available) were taken at baseline (week 0) and at week 20. We also obtained biopsies from three healthy individuals.

2015-12-08 | E-GEOD-74761 | biostudies-arrayexpress

Mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+)

2011-01-12 | GSE21568 | GEO

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.

2017-06-30 | GSE78722 | GEO

Transcriptome comparison of balding and non-balding dermal papilla aggregates from NHEK co-culturing

Project description:Androgenetic alopecia (AGA, male patterned baldness) is a prevalent hair loss condition in males that develops due to the influence of androgens and genetic predisposition. The keratinocytes-surrounded spheroid dermal papilla (DP) at the base of the hair follicle is essential in hair morphogenesis and cycling. With the aim of elucidating genes involved in AGA pathogenesis, we co-cultured immortalised balding and non-balding human DP cells (DPC) derived from male AGA patients with epidermal keratinocyte (NHEK) using multi-interfacial polyelectrolyte complexation (MIPC) technique, and compared gene expression using RNA-seq between isolated balding and non-balding DP aggregates.

2021-06-23 | GSE93766 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data