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Expression data from hair follicles treated with an osteopontin-derived peptide

ABSTRACT: Expression data from hair follicles treated with an osteopontin-derived peptide

PROVIDER: PRJNA420989 | ENA |

REPOSITORIES: ENA

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Expression data from hair follicles treated with an osteopontin-derived peptide

Project description:The human hair follicle is not only regulated, but is a source of transcription factors, hormones, neurohormones etc. which are crucial in regulating its growth. We used microarrays to determine the early response of microdissected human hair follicles to an osteopontin-derived peptide.

2017-12-05 | GSE107663 | GEO

FGF18 Signaling for Hair Cycle Resting Phase Determines Radioresistance of Hair Follicles by the Arrest of Hair Cycling

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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Hair follicles modulate skin barrier function

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RNAseq of organ-cultured human hair follicles exposed to MEKi (Cobimetinib)

Project description:EGFR/MEK inhibitor therapy induces a distinct inflammatory hair follicle response that includes a collapse of hair follicle immune privilege and differential modulation of IL-33 and IL-37 expression. Our findings suggest that successful future management of EGFRi/MEKi-induced folliculitis requires restoration of hair follicle immune privilege. In this RNAseq organ-cultured human hair follicles were directly exposed to MEKi (Cobimetinib) or the control DMSO (n=5 patients (6-8 hair follicles per patient)).

2024-07-19 | E-MTAB-13454 | biostudies-arrayexpress

Gene Expression in Unstaged Head Hair Follicles Plucked from Men and Women

Project description:Investigation of Gene Expression Profiling in Unstaged Head Hair Follicles Plucked from Men and Women Keywords: Gene Expression Profiling of Normal Hair Follicles

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Transcription profiling of mouse wildtype and Foxn1::dnFGFR2-IIIb transgenic hair follicles

Project description:rationale: comparison of gene expression profiles in wildtype and Foxn1::dnFGFR2-IIIb transgenic hair follicles; identification of targets that mediate the effects seen in transgenic hair follicles; results: as already suggested by the phenotype, the molecular abnormalities appear to be restricted to the hair shaft medulla; Igfbp5 is an important mediator of transgene-dependent effects

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Abnormalities in hair follicles of Pla2g2e knockout mice

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Human Hair follicles: Control Vs. 0.5 µM spermidine treatment

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Human Hair follicles: Control Vs. 0.5 µM spermidine treatment

Project description:To compare the effects of spermidine, key polyamine, on the gene expression profile of organ cultured human hair follicles Vehicle treated Vs. 0.5 µM spermidine treatment. Two control samples, two spermidine treated samples

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Mutational burden in human hair follicles

Project description:We would like to dissect human hair follicles and assess the mutations found in diffferent parts of the follicle eg bulge, root etc. We can also compare this with mutations found in the surrounding epidermis of the same patients (this is done under a different study). This may provide insights into the origin of PTCH1 mutants frequently seen in basal cell carcinoma but so far not located in our whole epidermis work as well as defining the clonality of the hair follicle

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