Regulatory T cells in skin promote hair follicle stem cell activation and hair growth through glucocorticoid signaling (ChIP-Seq)
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ABSTRACT:
PROVIDER: PRJNA762045 | ENA |
REPOSITORIES: ENA
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Project description:The maintenance of tissue homeostasis in steady state or under stress is dependent on the proper communication between tissue-resident stem cells (SCs) and immune cells in their microenvironment or “niche”. In addition to promoting immune tolerance, regulatory T cells (Tregs) have recently emerged as a critical component of stem cell niche in the hair follicle (HF), injured muscle, bone marrow and intestine to support stem cell differentiation. How Treg cells sense the dynamic signals in the niche environment and communicate with stem cells during tissue regeneration is largely unknown. Here, by using HF as a model, we uncover a hitherto unrecognized function of glucocorticoid receptor (GR) signaling pathway in skin-resident Treg cells to facilitate hair follicle stem cell (HFSC) activation and HF regeneration. Ablation of GR signaling in Tregs blocked HFSCs activation and proliferation after hair depilation and during the natural hair growth cycle. Mechanistically, GR signaling induces skin-resident Tregs to produce TGF-b3, which activates Smad2/3 in HFSCs and promotes HFSC proliferation and hair growth. Our study identifies a novel crosstalk between skin-resident Tregs and HFSCs mediated by the GR/TGF-b3 axis, highlighting a new avenue to manipulate Tregs to support tissue regeneration.
2022-05-02 | GSE183805 | GEO
Project description:The maintenance of tissue homeostasis in steady state or under stress is dependent on the proper communication between tissue-resident stem cells (SCs) and immune cells in their microenvironment or “niche”. In addition to promoting immune tolerance, regulatory T cells (Tregs) have recently emerged as a critical component of stem cell niche in the hair follicle (HF), injured muscle, bone marrow and intestine to support stem cell differentiation. How Treg cells sense the dynamic signals in the niche environment and communicate with stem cells during tissue regeneration is largely unknown. Here, by using HF as a model, we uncover a hitherto unrecognized function of glucocorticoid receptor (GR) signaling pathway in skin-resident Treg cells to facilitate hair follicle stem cell (HFSC) activation and HF regeneration. Ablation of GR signaling in Tregs blocked HFSCs activation and proliferation after hair depilation and during the natural hair growth cycle. Mechanistically, GR signaling induces skin-resident Tregs to produce TGF-b3, which activates Smad2/3 in HFSCs and promotes HFSC proliferation and hair growth. Our study identifies a novel crosstalk between skin-resident Tregs and HFSCs mediated by the GR/TGF-b3 axis, highlighting a new avenue to manipulate Tregs to support tissue regeneration.
2022-05-02 | GSE183804 | GEO
Project description:Regulatory T cells in skin promote hair follicle stem cell activation and hair growth through glucocorticoid signaling
| PRJNA762035 | ENA
Project description:Regulatory T cells in skin promote hair follicle stem cell activation and hair growth through glucocorticoid signaling (RNA-Seq)
| PRJNA762044 | ENA
Project description:Primary outcome(s): Comparison of the gene expression profile in hair follicle between cancer patients and healthy volunteer
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Project description:In this study, in order to explore the role of autophagy of human hair follicle stem cells in hair growth, we explored new ideas for hair regrowth. In this study, rapamycin was used to treat hair follicle stem cells to promote autophagy, and the different expression of genes was observed by comparing with the blank control group.
2024-01-10 | GSE229890 | GEO
Project description:Through phenotypical study, we found that miR-205 can promote hair growth. The goals of this study is to identify direct targets of miR-205 in hair follicle stem cells and determine whether and how miR-205 promotes hair growth by activating hair follicle stem cell.
2023-06-07 | GSE185116 | GEO
Project description:Hair follicles undergo recurrent cycling of controlled growth (anagen), regression (catagen), and relative quiescence (telogen) with a defined periodicity. Taking a genomics approach to study gene expression during synchronized mouse hair follicle cycling, we discovered that, in addition to circadian fluctuation, CLOCK-regulated genes are also modulated in phase with the hair growth cycle. During telogen and early anagen, circadian clock genes are prominently expressed in the secondary hair germ, which contains precursor cells for the growing follicle. Analysis of Clock and Bmal1 mutant mice reveals a delay in anagen progression, and the secondary hair germ cells show decreased levels of phosphorylated Rb and lack mitotic cells, suggesting that circadian clock genes regulate anagen progression via their effect on the cell cycle. Consistent with a block at the G1 phase of the cell cycle, we show a significant upregulation of p21 in Bmal1 mutant skin. While circadian clock mechanisms have been implicated in a variety of diurnal biological processes, our findings indicate that circadian clock genes may be utilized to modulate the progression of non-diurnal cyclic processes. To investigate the molecular control of hair follicle cycling, we profiled mRNA expression in mouse dorsal skin at multiple representative time points in the synchronized second postnatal hair growth cycle and in a depilation-induced hair growth cycle. For profiling of second synchronized and depilation-induced hair growth cycle, the same upper-mid region of dorsal skin was excised from C57BL/6 mice at representative postnatal days (P). The time points for second hair growth cycle are classified into different phases of the hair growth cycle based on established morphological guidelines as follow: early anagen (P23, P25), mid anagen (P27), late anagen (P29, P34), early catagen (P37, P39), mid catagen (P41), and telogen (P44). Depilation-induced hair growth cycle by applying wax/rosin mixture on the dorsal skin of seven-week old mice (all follicles in telogen) was performed on mice. The corresponding phases of the hair growth cycle at number of days following depilation (D) is as follow: early anagen (D3), mid anagen (D5), late anagen (D8, D12), and early catagen (D17). For each time point, multiple biological replicates were profiled, with each mouse dorsal skin separately hybridized to an Affymetrix array.
2009-07-17 | E-GEOD-11186 | biostudies-arrayexpress
Project description:Quiescent stem cells are periodically activated to maintain tissue homeostasis or occasionally called into action upon injury. Molecular mechanisms that constitutively maintain stem cell identity or promote stem cell proliferation and differentiation upon activation have been extensively studied. However, it is unclear how quiescent stem cells maintain identity and reinforce quiescence when they transition from quiescence to activation. Here we show mouse hair follicle stem cell compartment induces a transcription factor, Foxc1, when activated. Importantly, deletion of Foxc1 in the activated but not quiescent stem cells compromises stem cell identity, fails to re-establish quiescence and subsequently drives premature stem cell activation.These findings uncover a dynamic, cell-intrinsic mechanism employed by hair follicle stem cells to reinforce stemness in response to activation. Poly(A)-enriched transcriptome RNA-seq on HFSCs isolated in WT and K14Cre cKO mice at anagen and early telogen stage of hair cycle.
2016-02-05 | E-GEOD-67404 | biostudies-arrayexpress
Project description:miRNA profiling of human plucked hair follicle from frontal and occipital scalp
| EGAD00010001500 | EGA