TLDR Stat3 activation increases hair follicle progenitors but reduces bulge region stem cells.
The study investigated the effects of constitutive activation of Stat3 on hair follicle progenitor populations and bulge region keratinocyte stem cells (KSCs) in mice. It was found that in K5.Stat3C transgenic mice, which express an active form of Stat3, there was a significant reduction in CD34+ve/α6+ve KSCs in the bulge region compared to non-transgenic mice. Conversely, there was an increase in Sca-1 expressing cells in the hair follicle infundibulum. The activation of Stat3 led to the upregulation of Myc and cyclin D1, and a reduction in α6 and β1 integrin levels, suggesting that Stat3 activation causes stem cells to exit the bulge region. This indicated that Stat3 played a crucial role in regulating the behavior and growth properties of bulge region KSCs.
95 citations
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July 2006 in “British Journal of Dermatology” 45 citations
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April 2001 in “The journal of investigative dermatology/Journal of investigative dermatology” Different Myc family proteins are located in various parts of the hair follicle and may affect stem cell behavior.
10 citations
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October 2000 in “PubMed” The study investigated the effects of expressing human papillomavirus type 16 E6/E7 oncogenes in the outer root sheath of hair follicles in transgenic mice. These mice exhibited a fur phenotype with lower hair density but faster hair regeneration compared to wild-type mice. The expression of these oncogenes extended the growth phase (anagen) of hair follicles and bypassed the resting phase (telogen), leading to continuous hair follicle cycling. Although the first hair growth cycle appeared normal, the second cycle showed delayed initiation of catagen and insensitivity to telogen resting signals, even with estradiol present. This indicated that E6/E7 expression in the ORS delayed catagen entry and prevented telogen rest, resulting in ongoing hair follicle cycling.
69 citations
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May 1997 in “Veterinary Pathology” The angora mouse mutation causes long hair and hair defects due to a gene deletion.
128 citations
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February 1992 in “British Journal of Dermatology” Basal cell carcinomas likely originate from hair follicle cells or stem cells.