Next generation sequence analysis of cells derived from mouse hair follicles after long term culture
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE201445 | GEO | 2022/06/30
REPOSITORIES: GEO
Similar Datasets
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
Project description:Aging organs functionally and structurally decline with the loss of their regenerative capabilities, yet the existence of distinct cell division programs that determine organ fates is unknown. Hair follicles, mammalian mini-organs that grow hair, miniaturize by aging. Here we report that hair follicle regeneration and aging are driven by distinct cell division types of hair follicle stem cells (HFSCs). Cell fate tracing and cell division axis analysis in mice revealed that HFSCs undergo symmetric and asymmetric cell divisions to generate a new bulge, yet preferentially provoke “stress-responsive type” asymmetric cell divisions that generate aberrantly differentiating cells upon age/stress. That dynamic program with repetitive divisions efficiently eradicates those cells through defective association and stabilization of a hemidesmosomal protein COL17A1 and a cell-polarity-protein aPKCλ in HFSCs, thereby causing organ aging. The forced stabilization of COL17A1 rescued organ aging through aPKCλ stabilization. These results demonstrate that distinct cell division programs govern tissue/organ fates.
2020-12-25 | GSE124119 | GEO
Project description:Mechanisms of plasticity to acquire different cell fates are critical for adult stem cell (SC) potential, yet are poorly understood. Reduced global histone methylation is an epigenetic state known to mediate plasticity in cultured embryonic SCs and T cell progenitors. We used mouse hair follicle stem cells (HFSCs) at two different hair cycle stages (early anagen and late catagen) to compare the genome-wide changes in the levels of histone modification marks H3K4me3, H3K9me3, and H3K27me3. Hair follicle stem cells from Early Anagen (EA-HFSCs) and Late Catagen (LC-HFSCs), and their non-HFSCs counterparts (nEA-HFSCs and nLC-HFSCs), were FACS-isolated for Chromatin Immunoprecipitation followed by sequencing (ChIP-seq) analysis of H3K4me3, H3K9me3, and H3K27me3.
2016-04-13 | E-GEOD-78749 | biostudies-arrayexpress
Project description:Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by hair follicle stem cells (HFSCs). HFSCs regenerate hair in response to canonical Wnt signalling. We used RNA-seq to unfold genome-wide chromatin landscapes of β-catenin within the native HFSC-niche.
2013-12-03 | GSE48878 | GEO
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
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
Project description:The use of dermal papilla cells for hair follicle (HF) regeneration is long accepted much attention. However, cultured dermal papilla cells tend to lose the hair-inducible capability during passaging, which restricts its application. Increasing evidences indicate that dermal papilla cells exert their regulatory function of HF growth mainly through their unique paracrine properties, opening up a way to exosome therapies.This study aimed to explore the effects of exosomes from high and low-passaged human scalp follicle dermal papilla cells (DP-Exos) on hair follicle stem cells (HFSCs) activation and hair growth, and to investigate the underline mechanism. DP-Exos were isolated by ultracentrifugation and cultured with human scalp follicles and HFSCs. The hair elongation and cell proliferation was assessed. Quantitative real-time PCR (qRT-PCR) and Western-blot were performed to detect the expression levels of a class of miRNAs and proteins which have positive roles in regulating hair growth and HFSCs proliferation. High throughput miRNA sequencing of miRNAs in high (P8) and low-passaged (P3) DP-Exos was performed, and the utmost miRNA and its target gene was identified via bioinformatics analysis.
2021-01-13 | GSE136241 | GEO
Project description:Obesity, a worldwide epidemic, predisposes to many ageing-associated diseases, yet its exact impact on organ dysfunction is largely unknown. Hair follicles, mini-epithelial organs that grow hair, miniaturize by ageing to cause hair loss through the depletion of hair follicle stem cells (HFSCs). Here, we report that obesity-induced stress such as by high-fat diet (HFD) feeding primarily targets HFSCs to accelerate hair thinning. Chronological gene expression analysis revealed that HFD feeding for four consecutive days directs activated HFSCs toward epidermal keratinization by generating excessive reactive oxygen species yet retains HFSC pools in young mice. Integrative analysis with stem cell fate tracing, epigenetic analysis and reverse genetics revealed that further feeding of HFD subsequently induces lipid droplets and NF-κB activation within HFSCs via autocrine/paracrine IL1R signaling. Those integrated factors converge on the profound inhibition of Sonic hedgehog (Shh) signal transduction in HFSCs, thereby further depleting lipid-laden HFSCs from the skin surface and inducing hair follicle miniaturization and eventual hair loss. Conversely, Shh activation by transgenes or compounds rescues HFD-induced hair loss. These data collectively demonstrate that stem cell inflammageing induced by obesity robustly represses organ regeneration signals to accelerate the mini-organ miniaturization, and indicates suggests the importance of daily prevention of organ dysfunction.
2021-04-14 | GSE131958 | GEO
Project description:Hair loss is one of the typical aging phenotypes in mammals, yet the underlying mechanism(s) is unclear. Here we report that hair follicle stem cell (HFSC) aging causes the stepwise miniaturization of hair follicles and eventual hair loss both in wild-type mice and in humans. In vivo fate analysis of HFSCs revealed that the DNA damage response in HFSCs causes proteolysis of Type XVII Collagen (COL17A1/BP180) to trigger “HFSC aging”, characterized by their loss of stemness signature and epidermal commitment. Those aged HFSCs are cyclically eliminated from the skin through their terminal epidermal differentiation, thereby causing hair follicle miniaturization. That process can be recapitulated by Col17a1 deficiency and prevented by forced maintenance of COL17A1 in HFSCs, demonstrating that stem cell homeostasis is the keystone against ultimate execution of the tissue/organ aging program.
2015-12-01 | GSE72863 | GEO
Project description:Obesity, a worldwide epidemic, predisposes to many ageing-associated diseases, yet its exact impact on organ dysfunction is largely unknown. Hair follicles, mini-epithelial organs that grow hair, miniaturize by ageing to cause hair loss through the depletion of hair follicle stem cells (HFSCs). Here, we report that obesity-induced stress such as by high-fat diet (HFD) feeding primarily targets HFSCs to accelerate hair thinning. Chronological gene expression analysis revealed that HFD feeding for four consecutive days directs activated HFSCs toward epidermal keratinization by generating excessive reactive oxygen species yet retains HFSC pools in young mice. Integrative analysis with stem cell fate tracing, epigenetic analysis and reverse genetics revealed that further feeding of HFD subsequently induces lipid droplets and NF-B activation within HFSCs via autocrine/paracrine IL1R signaling. Those integrated factors converge on the profound inhibition of Sonic hedgehog (Shh) signal transduction in HFSCs, thereby further depleting lipid-laden HFSCs through their aberrant differentiation and inducing hair follicle miniaturization and eventual hair loss. Conversely, Shh activation by transgenes or compounds rescues HFD-induced hair loss. These data collectively demonstrate that stem cell inflammageing induced by obesity robustly represses organ regeneration signals to accelerate the mini-organ miniaturization, and suggests the importance of daily prevention of organ dysfunction.
2021-04-14 | GSE169173 | GEO