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Publication : Integrin β6-deficient mice show enhanced keratinocyte proliferation and retarded hair follicle regression after depilation.

First Author  Xie Y Year  2012
Journal  J Invest Dermatol Volume  132
Issue  3 Pt 1 Pages  547-55
PubMed ID  22113470 Mgi Jnum  J:183167
Mgi Id  MGI:5317974 Doi  10.1038/jid.2011.381
Citation  Xie Y, et al. (2012) Integrin beta6-deficient mice show enhanced keratinocyte proliferation and retarded hair follicle regression after depilation. J Invest Dermatol 132(3 Pt 1):547-55
abstractText  Integrin alphavbeta6 is an epithelial-specific receptor that binds and activates latent transforming growth factor-beta1 (TGF-beta1). TGF-beta1 has been implicated as an endogenous inducer of hair follicle (HF) regression during hair cycling. We hypothesized that alphavbeta6 integrin-mediated TGF-beta1 signaling regulates hair regeneration and HF involution. In wild-type (WT) mice, the expression of integrin alphavbeta6 was strongly upregulated in the outer root sheath (ORS) during early hair regeneration, and was specifically enhanced in the HF bulge region. Expression gradually decreased in late anagen and remained restricted to the bulge region in the catagen and telogen stage HFs. The first spontaneous hair cycle was not altered in beta6 integrin knockout (beta6(-/-)) mice. However, after depilation, beta6(-/-) mice exhibited retarded HF regression compared with WT controls. beta6(-/-) follicles contained significantly higher numbers of proliferating Ki67-positive keratinocytes than WT follicles at an identical cycle stage. The beta6(-/-) follicles also demonstrated significantly reduced levels of TGF-beta1 expression and Smad2 phosphorylation during early anagen and anagen-catagen transition. Our study indicates that alphavbeta6 integrin has an important inhibitory role in keratinocyte proliferation in both HFs and interfollicular epidermis. Thus, downregulated TGF-beta1 signaling in beta6(-/-) mice may affect bulge niche stem cell behavior.
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