Abstract
Enhanced telomerase reverse transcriptase (TERT) levels in dermal keratinocytes can serve as a novel target for hair growth promotion. Previously, we identified fisetin using a system for screening food components that can activate the TERT promoter in HaCaT cells (keratinocytes). In the present study, we aimed to clarify the molecular basis of fisetin-induced hair growth promotion in mice. To this end, the dorsal skin of mice was treated with fisetin, and hair growth was evaluated 12 days after treatment. Histochemical analyses of fisetin-treated skin samples and HaCaT cells were performed to observe the effects of fisetin. The results showed that fisetin activated HaCaT cells by regulating the expression of various genes related to epidermogenesis, cell proliferation, hair follicle regulation, and hair cycle regulation. In addition, fisetin induced the secretion of exosomes from HaCaT cells, which activated β-catenin and mitochondria in hair follicle stem cells (HFSCs) and induced their proliferation. Moreover, these results revealed the existence of exosomes as the molecular basis of keratinocyte-HFSC interaction and showed that fisetin, along with its effects on keratinocytes, caused exosome secretion, thereby activating HFSCs. This is the first study to show that keratinocyte-derived exosomes can activate HFSCs and consequently induce hair growth.
Highlights
IntroductionPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
Fisetin regulated the expression of various genes, such as those encoding secretory factors and those involved in epidermogenesis, cell proliferation, hair follicle regulation, and hair cycle regulation (Tables 1 and 2)
We reported that fisetin, which augments the expression of telomerase reverse transcriptase (TERT)
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Telomerase reverse transcriptase (TERT) maintains telomere length and is known to be active in stem cells as well as cancer cells. Sarin et al (2005) reported that when. TERT is transgenically introduced into mouse skin, the hair follicle cycle shifts from the telogen phase, the quiescent phase, to the anagen phase, the active phase, resulting in hair growth [1]. The overexpression of TERT induces the proliferation of hair follicle stem cells (HFSCs) in the bulge region, leading to hair growth.
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