Stabilization of the hair cycle
Control of the hair cycle
Numerous, poorly understood endocrine, autocrine, and paracrine signaling mechanisms interact intricately to regulate the hair cycle. The Wnt family is noteworthy in particular, and the precise roles that its members play are yet unclear. Beta-catenin is a fundamental component of the Wnt signaling pathway and is necessary for the differentiation of stem cells into follicular keratinocytes28. The change from anagen to telogen is brought about by temporary β-catenin signaling29,30, and is impacted by the cyclical production of bone morphogenic proteins (BMP2 and 4), which are made by subcutaneous adipocytes and dermal fibroblasts31, and by fibroblast growth factors (FGF 7 and 10),Wnt7b31,33–36 and BMP inhibitors, such as transforming growth factor b2 [TGF-b2] and noggin. Furthermore, platelet-derived growth factor (PDGF) alpha is produced by adipocyte precursor cells, which activates the PDGF receptor in the DP and causes hair germ activation37. Perifollicular vascularization has been demonstrated to rise during anagen and decrease during catagen, and it is associated with over- and under-expression of the ORS keratinocyte vascular endothelial growth factor (VEGF) mRNA, respectively38. Insulin-like growth factor 1 (IGF-1) has been found to be a key regulator in the hair follicle41,42, while hepatocyte growth factor/scatter factor has been demonstrated to stimulate hair follicle growth in vitro39,40.
Nanosized extracellular phospholipid bilayer membranous vesicles (exosomes 30–120 nm and microvesicles 100–1000 nm) that can transport lipids, metabolites, nucleic acids, and proteins have been identified over the past ten years as a therapeutically relevant new method of paracrine signaling43–45. Zhou and colleagues found that in mice models, DP cell-exosomes extracted from healthy human scalp specimens sped up the anagen phase and postponed the catagen phase, leading to elevated levels of β-catenin and Sonic hedgehog (Shh)46. Human dermal papillae exposed to activated human dermal fibroblasts (hDFs) secrete the non-Wnt ligand Norrin43 through stimulated extracellular vesicles, or st-EVs, according to a recent study. The hypothesis is that the particular receptor for Norrin, Frizzled-4 (Fzd4), given by hDF, enhances the subsequent activation of the β-catenin pathway, leading to the identified.
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