The Epithelial Stem Cell Niche in Skin

This study found that macrophages near hair follicles contribute to the activation of skin epithelial stem cells in mice, suggesting a novel role for macrophages in regulating hair growth.

In this study, mouse sweat gland development relied on a regulatory sequence initiated by Wnt/β-catenin signaling, and disruptions in Wnt, Eda, or Shh pathways led to distinct developmental failures.

This study found that skin fibroblasts in mice arise from two distinct lineages which contribute differently to dermal structure and repair, impacting hair follicle formation during wound healing.

This study found that fibroblast growth factor 9, initially secreted by γδ T cells, plays a key role in modulating hair follicle regeneration in mice after skin wounds.

Hair follicle stem cells rely on nearby blood vessels for their maintenance and function.

This study found that TGFβ signaling is essential for keeping sebocytes undifferentiated by reducing lipid-related gene expression, using a novel human sebocyte culture model.

This study found multipotent progenitors in sweat ducts that become unipotent after sweat gland development, highlighting distinct regenerative capabilities in adult glandular skin stem cell populations.

This study demonstrates the potential of using bioengineered follicles from adult tissue-derived stem cells for fully functional hair regeneration, illustrating possible applications in organ replacement therapy.

This study found that intradermal adipocyte lineage cells in mice are necessary and sufficient to activate follicular stem cells, highlighting their role in regulating skin stem cell activity.

This study demonstrates that hair follicle bulge stem cells can transition into other stem cell compartments, indicating their role in maintaining both hair follicles and sebaceous glands.

This study found that Wnt signaling in the hair follicle is crucial for coordinating the behavior of epithelial and melanocyte stem cells, which drives hair regeneration and melanocyte differentiation in mice.

This study found that Shh from neurons signals to Gli1-expressing cells in the hair follicle, cultivating a niche where these bulge cells can potentially transform into epidermal stem cells in wound healing.

This study found that abolishing H3K27me3 in mouse skin by targeting Ezh2 and Ezh1 affects hair follicle development and epidermal behavior, revealing functional differences between these tissues.

COL17A1 is crucial for preventing hair graying and loss by supporting hair and pigment stem cells.

Nephronectin helps attach muscle cells to hair follicles.

This study identified key genetic regions associated with alopecia areata, highlighting both acquired and innate immune involvement, with a novel link to the upregulation of ULBP ligands in autoimmune disease.

This study found that in mice, inactivating beta-catenin in the dermal papilla reduces hair follicle progenitor proliferation and disrupts the hair cycle.

This review discusses the development and advances in studying trichogenic dermal cells for hair follicle morphogenesis, summarizing methods, bioassays, and molecular markers, but reports no new research findings.

This study suggests that Lrig1-positive cells form a previously unknown reservoir of interfollicular epidermal stem cells in adult mouse skin, influencing epidermal proliferation and hair follicle development.

This review highlights recent findings on the importance of signalling pathways in sebaceous gland morphogenesis and differentiation, but reports no new clinical results.

This study found that disrupting Smad4 signaling in young mice led to overactivation of follicle stem cells, causing hyperplasia and depletion of the stem cell niche.

Lgr5 is a marker for active, long-lasting stem cells in mouse hair follicles.

NFATc1 controls hair stem cell activity, affecting hair growth and could be a target for hair loss treatments.

This study found that Smad7 perturbs hair follicle development while promoting sebaceous gland formation by antagonizing Wnt/β-catenin signaling in transgenic mice.

This study developed molecular signatures for dermal papilla cells and their niche, uncovering novel signaling regulators and genes linked to hair disorders, which may inform future hair development research.

This study found that stabilized beta-catenin is crucial for activating stem cell transition from quiescence to proliferation in hair follicles by influencing gene expression within the stem cell niche.

This study found that continuous β-catenin signaling in adult mouse epidermis can reprogram hair follicles to form benign tumors, which regress after the signaling is discontinued.

The K15 promoter effectively targets stem cells in the hair follicle bulge.

This study concluded that label-retaining cells in mouse epidermis differ in their sensitivity to proliferative stimuli, influencing their division and potential transdifferentiation without consistently depleting their population.

CD34 is a marker for isolating stem-like cells in mouse hair follicles.

The Dfl mutation in mice causes poor sebaceous gland function and complete hair loss.

This study observed that hair follicle innervation in C57BL/6 mice occurs in sequential stages that closely correlate with the development of hair follicles, indicating an interdependent relationship between neuronal and epithelial morphogenesis.

This study found that LEF1/TCF3 is necessary but not sufficient for TOPGAL activation in hair follicle development, indicating complex regulation in the skin.