Similar Datasets
Project description:The ability of tissue stem cells to sense and respond to their surroundings enables them to adapt their activity to meet the needs of the organism. External irritation has long been observed in humans to cause acquired hypertrichosis, but the mechanism is unknown. We discovered that external irritation activates hair follicle stem cells (HFSCs), leading to substantial hair regeneration in mice. The external irritation is sensed by niche adipocytes, which undergo lipolysis to activate HFSCs, rather than by the HFSCs themselves. Fatty acids released by adipocytes are taken up by HFSCs and activate them by priming them for fatty acid oxidation and increasing the mitochondrial oxidative phosphorylation capacity for ATP production. Inhibiting lipolysis, fatty acid uptake, or fatty acid oxidation restricts irritation-induced hair regeneration. As a result, adipocytes create an injury-sensing niche, allowing HFSCs to respond to external irritation by initiating a new round of hair growth to protect the skin.
2025-11-13 | GSE295606 | GEO
Project description:The ability of tissue stem cells to sense and respond to their surroundings enables them to adapt their activity to meet the needs of the organism. External irritation has long been observed in humans to cause acquired hypertrichosis, but the mechanism is unknown. We discovered that external irritation activates hair follicle stem cells (HFSCs), leading to substantial hair regeneration in mice. The external irritation is sensed by niche adipocytes, which undergo lipolysis to activate HFSCs, rather than by the HFSCs themselves. Fatty acids released by adipocytes are taken up by HFSCs and activate them by priming them for fatty acid oxidation and increasing the mitochondrial oxidative phosphorylation capacity for ATP production. Inhibiting lipolysis, fatty acid uptake, or fatty acid oxidation restricts irritation-induced hair regeneration. As a result, adipocytes create an injury-sensing niche, allowing HFSCs to respond to external irritation by initiating a new round of hair growth to protect the skin.
2025-11-13 | GSE239988 | GEO
Project description:The ability of tissue stem cells to sense and respond to their surroundings enables them to adapt their activity to meet the needs of the organism. External irritation has long been observed in humans to cause acquired hypertrichosis, but the mechanism is unknown. We discovered that external irritation activates hair follicle stem cells (HFSCs), leading to substantial hair regeneration in mice. The external irritation is sensed by niche adipocytes, which undergo lipolysis to activate HFSCs, rather than by the HFSCs themselves. Fatty acids released by adipocytes are taken up by HFSCs and activate them by priming them for fatty acid oxidation and increasing the mitochondrial oxidative phosphorylation capacity for ATP production. Inhibiting lipolysis, fatty acid uptake, or fatty acid oxidation restricts irritation-induced hair regeneration. As a result, adipocytes create an injury-sensing niche, allowing HFSCs to respond to external irritation by initiating a new round of hair growth to protect the skin.
2025-11-13 | GSE239986 | GEO
Project description:The ability of tissue stem cells to sense and respond to their surroundings enables them to adapt their activity to meet the needs of the organism. External irritation has long been observed in humans to cause acquired hypertrichosis, but the mechanism is unknown. We discovered that external irritation activates hair follicle stem cells (HFSCs), leading to substantial hair regeneration in mice. The external irritation is sensed by niche adipocytes, which undergo lipolysis to activate HFSCs, rather than by the HFSCs themselves. Fatty acids released by adipocytes are taken up by HFSCs and activate them by priming them for fatty acid oxidation and increasing the mitochondrial oxidative phosphorylation capacity for ATP production. Inhibiting lipolysis, fatty acid uptake, or fatty acid oxidation restricts irritation-induced hair regeneration. As a result, adipocytes create an injury-sensing niche, allowing HFSCs to respond to external irritation by initiating a new round of hair growth to protect the skin.
2025-11-13 | GSE295605 | GEO
Project description:Dermal adipocytes activate hair follicle stem cells through metabolic communication
| PRJNA1001872 | ENA
Project description:Dermal adipocytes activate hair follicle stem cells through metabolic communication [HFSC]
| PRJNA1001882 | ENA
Project description:Dermal adipocytes activate hair follicle stem cells through metabolic communication [SDS]
| PRJNA1001881 | ENA
Project description:Hair follicle stem cells in the epithelial bulge are responsible for the continual regeneration of the hair follicle during cycling. The bulge cells reside in a niche composed of dermal cells. The dermal compartment of the hair follicle consists of the dermal papilla and dermal sheath. Interactions between hair follicle epithelial and dermal cells are necessary for hair follicle morphogenesis during development and in hair reconstitution assays. Dermal papilla and dermal sheath cells express specific markers and possess distinctive morphology and behavior in culture. These cells can induce hair follicle differentiation in epithelial cells and are required in hair reconstitution assays either in the form of intact tissue, dissociated freshly prepared cells or cultured cells. This review will focus on hair follicle dermal cells since most therapeutic efforts to date have concentrated on this aspect of the hair follicle, with the idea that enriching hair-inductive dermal cell populations and expanding their number by culture while maintaining their properties, will establish an efficient hair reconstitution assay that could eventually have therapeutic implications.
| S-EPMC2818774 | biostudies-literature
Project description:Hair follicle (HF) growth and development are controlled by various cell types, including hair follicle stem cells (HFSCs) and dermal papilla cells (DPCs). Exosomes are nanostructures that participate in many biological processes. Accumulating evidence indicates that DPC-derived exosomes (DPC-Exos) mediate HFSC proliferation and differentiation during the cyclical growth of hair follicles. In this study, we found that DPC-Exos increase ki67 expression and CCK8 cell viability readouts in HFSCs but reduce annexin staining of apoptotic cells. RNA sequencing of DPC-Exos-treated HFSCs identified 3702 significantly differentially expressed genes (DEGs), including BMP4, LEF1, IGF1R, TGFβ3, TGFα, and KRT17. These DEGs were enriched in HF growth- and development-related pathways. We further verified the function of LEF1 and showed that overexpression of LEF1 increased the expression of HF development-related genes and proteins, enhanced HFSC proliferation, and reduced HFSC apoptosis, while knockdown of LEF1 reversed these effects. DPC-Exos could also rescue the siRNA-LEF1 effect in HFSCs. In conclusion, this study demonstrates that DPC-Exos mediated cell-to-cell communication can regulate HFSCs proliferation by stimulating LEF1 and provide novel insights into HF growth and development regulatory mechanisms.
| S-EPMC9964005 | biostudies-literature
Project description:Hair follicle stem cells (HFSCs) and dermal papilla cells (DPCs) are crucial in the biogenesis and maintenance of hair follicles (HFs). This study demonstrated that a fragment derived from aminoacyl-tRNA synthetase-interacting multifunctional protein1 (AIMP1) secreted from HFSCs activated DPCs and maintained HF homeostasis. A histological analysis revealed that AIMP1 levels in HF decreased with hair loss. Hair regrowth in AIMP1-induced mice was faster than in non-induced mice. Deletion mapping revealed 41 amino acids (TN41, aa 6-46) as the active region of AIMP1. The N-terminal peptide fragment of AIMP1 generated by MMP1 was secreted from Wnt-treated HFSCs to activate DPCs. TN41 activated Akt and ERK, increased β-catenin, and enhanced DPC activation. TN41 promoted hair shaft elongation in cultured human HFs and improved the hair-inducing activity of cultured DPC spheroids. Our findings suggest that the AIMP1 fragment secreted from HFSCs stimulates active hair regrowth through activating DPCs.
| S-EPMC11528461 | biostudies-literature