Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hair growth is induced by blockade of macrophage-derived oncostatin M and JAK-STAT5 signaling in hair follicle stem cells.

ABSTRACT: We also show that OSM is sufficient for maintaining quiescence of hair follicle stem cells (HFSCs), and OSMRβ-JAK-STAT5 signaling is necessary for maintaining the resting phase of the hair cycle (telogen). Using single-cell RNA sequencing, we identify the source of OSM to be a distinct subset of TREM2+ macrophages that predominate during early telogen. Moreover, inhibition of macrophages during telogen by genetic ablation, neutralizing antibodies and small-molecule inhibitors was sufficient to induce anagen.

ORGANISM(S): Mus musculus

PROVIDER: GSE108709 | GEO | 2019/04/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Paracrine TGFß Signaling Counterbalances BMP-Mediated Repression in Hair Follicle Stem Cell Activation

Project description:Hair follicle (HF) regeneration begins when communication between quiescent epithelial stem cells (SCs) and underlying mesenchymal dermal papillae (DP) generates sufficient activating cues to overcome repressive BMP signals from surrounding niche cells. We uncovered a hitherto unrecognized DP transmitter, TGFβ2, which activates Smad2/3 transiently in HFSCs concomitant with entry into tissue regeneration. We used microarrays to detect the genes specifically affected by TGFß receptor II-deficient mice upon HFSC activation. Hair follicle stem cells (HFSCs) of hair gem (HG) and bulge, and total skin keratinocytes were FACS-purified from the mouse back skin at 2nd telogen-to-anagen transition stages.

2012-01-04 | E-GEOD-33471 | biostudies-arrayexpress

Nfatc1 Orchestrates Aging in Hair Follicle Stem Cells

Project description:Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by hair follicle stem cells (HFSCs). We used ChIP-seq to unfold genome-wide chromatin landscapes of Nfatc1 and dissect the biological relevence of its upstream BMP signaling in HFSC aging. Telogen quiescent hair follicle stem cells (HFSCs) were FACS-purified for ChIP-sequcencing.

2013-11-14 | E-GEOD-52328 | biostudies-arrayexpress

Stem cell quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors

Project description:In many organs, adult stem cells are uniquely poised to serve as cancer cells of origin. In the epidermis, hair follicle stem cells (HFSCs) cycle through stages of quiescence (telogen) and proliferation (anagen) to drive hair growth. Within the hair follicle, HFSCs are capable of initiating squamous cell carcinoma, yet it is unclear how the hair cycle contributes to tumorigenesis. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to gain of oncogenes (Ras) or loss of tumor suppressors (p53). Instead, prolonged oncogenic stimuli only exert their effects when HFSC quiescence mechanisms are removed by normal HFSC activation. Furthermore, Pten activity is necessary for quiescence based tumor suppression, since Pten deletion alleviates this stem cell specific ability without affecting proliferation per se. Small RNAs were cloned from Trizol-lysed cells sorted from mouse skin and sequenced with the Illumina HiSeq2000.

2013-10-28 | E-GEOD-51765 | biostudies-arrayexpress

Stem cell quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors

2013-10-28 | GSE51765 | GEO

RNA-seq analysis of hair follicle stem cell transcriptome upon loss of the transcription factor FOXC1

Project description:We report downstream gene expression changes in stem cells of the adult mouse hair follicle upon conditional ablating of the transcription factor Forkhead Box C1 transcription factor (FOXC1). Hair follicles undergo cycles of rest (telogen; Tel) and regeneration (anagen; Ana). As such, we performed our analysis on these two different stages of hair follicles. mRNA-sequencing of WT vs. Foxc1-conditional or inducible KO (Foxc1-cKO or iKO) hair follicle stem cells (HFSCs) purified from mouse dorsal back skin by flow-activated cell sorting (FACS).

2016-02-16 | E-GEOD-77256 | biostudies-arrayexpress

SOX9: a Stem Cell Transcriptional Regulator of Secreted Niche Signaling Factors

Project description:Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by hair follicle stem cells (HFSCs). We used RNA-seq to identify SOX9-dependent transcriptional changes and ChIP-seq to identify SOX9-bound genes in HF-SCs. Telogen quiescent hair follicle stem cells (HFSCs) and intefollicular epidermal cells (IFE) were FACS-purified for ChIP-sequcencing and HFSCs for RNA-Sequencing

2014-01-28 | E-GEOD-54424 | biostudies-arrayexpress

Hair folicle-qSC-pSC-TEL-ANA-compare

Project description:It was shown that HF stem cells (HFSCs) also consist of two functionally distinct pSCs and qSCs. In telogen, qSCs are located in the bulge area and the pSCs are housed in secondary hair germ right above dermal papilla cells. These two populations respond differently to the regenerative signals during hair regeneration.

2021-11-19 | PXD013028 | JPOST Repository

Gene expression profile of hair follicle stem cells (HFSCs) isolated from wild type and homozygous Dab2 cKO (Dab2 Fl/Fl) mice at postnatal day 35

Project description:Disabled 2 is an endocytic adaptor protein known to regulate various signaling pathways such Wnt , BMP, TGF and Ras/MAPK. In the present study, we observed that Dab2 is expressed in all the compartments of the hair follicle. K14 Cre specific homozygous Dab2 knockout resulted in delayed activation of HFSCs and delayed Ist hair follicle cycle initiation. At PD35, while WT progresses to anagen II, the Dab2 cKO mice still remains at telogen. In addition, loss of Dab2 alos led to reduced HFSCs pool extended quiescence, and reduced self renewal capacity of HFSCs at PD35. We performed expression profiling of HFSCs isolated from WT and Dab2 cKO mice at PD35 to check for the differentially regulated genes involved in HFSCs activation. The expression analysis helped us to elucidate the detailed molecular mechanisms involved in Dab2 mediated regulation of HFSCs activation and quiescence.

2024-03-01 | GSE250300 | GEO

Gene expression profile of hair follicle stem cells (HFSCs) isolated from wild type and homozygous Dab2 cKO (Dab2 Fl/Fl) mice at postnatal day 68

Project description:Disabled 2 is an endocytic adaptor protein known to regulate various signaling pathways such Wnt , BMP, TGF and Ras/MAPK. In the present study, we observed that Dab2 is expressed in all the compartments of the hair follicle. K14 Cre specific homozygous Dab2 knockout resulted in delayed activation of HFSCs and delayed Ist hair follicle cycle initiation. At PD68, both WT and Dab2 cKO mice were at telogen. In addition, loss of Dab2 also led to reduced HFSCs pool extended quiescence, and reduced self renewal capacity of HFSCs at PD68. We performed expression profiling of HFSCs isolated from WT and Dab2 cKO mice at PD68 to check for the differentially regulated genes involved in HFSCs activation. The expression analysis helped us to elucidate the detailed molecular mechanisms involved in Dab2 mediated regulation of HFSCs activation and quiescence.

2024-03-31 | GSE254311 | 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.

2017-06-03 | GSE69501 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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