Profiling the response of scalp hair follicles to short-term treatment with hepatocyte growth factor
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ABSTRACT:
PROVIDER: PRJNA636366 | ENA |
REPOSITORIES: ENA
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Project description:Hepatocyte growth factor (HGF) is a well-known promoter of cell proliferation, morphogenesis, migration, angiogenesis and pigmentation. To characterize its effects on human scalp dissected hair follicles, we performed gene expression profiling on RNA isolated from entire hair follicles, comparing the effects of 6hr HGF treatment versus control. 183 genes were differentially up-/down-regulated compared to vehicle control. These genes were involved in a number of different biological pathways suggesting that HGF can have various effects upon human hair follicle function.
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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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Project description:RNA-seq data of human scalp hair follicles following SEP1 phage treatment
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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.
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Project description:Investigation of Gene Expression Profiling in Unstaged Head Hair Follicles Plucked from Men and Women Experiment Overall Design: Total RNA was extracted from 1-3 unstaged follicles plucked from the scalp of each of 36 adult human volunteers. The average quantifiable yield of RNA per follicle was 112.5 ng. Ten samples were selected, based on ribosomal ratio, relative integrity number and total yield, for expression profiling. By preamplifying the extracted RNA (starting with as little as 30 ng), sufficient labeled RNA was generated to conduct Afymetrix-based gene expression analysis.
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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.
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Project description:When faced with clinical symptoms of scarring alopecia – the standard diagnostic pathway involves a scalp biopsy which is an invasive and expensive procedure. Furthermore, clinical activity of scarring alopecias is often difficult to assess as symptoms of permanent damage and signs of activity can overlap or be difficult to distinguish. Here we report that gene expression analysis of only a small number of hair follicles (HF) plucked from lesional areas of the scalp is sufficient to characterise chronic discoid lupus erythematosus (CDLE). Lesional and non-lesional HFs were extracted from the scalp of patients with CDLE, psoriasis and healthy controls. The expression profile from CDLE HFs coincides with published profiles of CDLE from skin biopsy and was consistent with histopathological diagnostic features of CDLE. We therefore propose that information obtained from this non-invasive approach are sufficient to diagnose scalp LE.
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Project description:Human hair follicles from normal areas of the scalp were disassociated to single cells, sorted and tested by microarrray To compare the expression of human CD200+ CD49+ hair follicle keratinocytes versus CD200-CD49+ keratinocytes
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Project description:Telogen (resting phase) hair follicles are more radioresistant than anagen (growth phase) ones. Irradiation of BALB/c mice in the anagen phase with γ-rays at 6 Gy induced hair follicle dystrophy, whereas irradiation in the telogen phase induced the arrest of hair follicle elongation without any dystrophy after post-irradiation depilation. In contrast, FGF18 was highly expressed in the telogen hair follicles to maintain the telogen phase and also the quiescence of hair follicle stem cells. Therefore, the inhibition of FGF receptor signaling at telogen induced the dystrophy after post-irradiation depilation. In addition, the administration of recombinant FGF18 suppressed cell proliferation in the hair follicles and enhanced the repair of radiation-induced DNA damage, so FGF18 protected the anagen hair follicles against radiation damage to enhance hair regeneration. Moreover, FGF18 reduced the expression of cyclin B1 and cdc2 in the skin and FGF18 signaling induced G2/M arrest in the keratinocyte cell line HaCaT, although no obvious change of the expression of DNA repair genes was detected by DNA microarray analysis. These findings suggest that FGF18 signaling for the hair cycle resting phase causes radioresistance in telogen hair follicles by arresting the proliferation of hair follicle cells.
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