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. Author manuscript; available in PMC: 2015 Jun 1.
Published in final edited form as: Exp Dermatol. 2014 Jun;23(6):407–413. doi: 10.1111/exd.12416

Figure 2.

Figure 2

Wnt10b-induced hair follicles were accompanied by excessive activation of the Wnt/β-catenin pathway, increased proliferation, and hair stem cell activation and migration. a-b. Immunostaining and statistical chart showed nuclear β-catenin, a key mediator of the Wnt signaling pathway, was dramatically increased in the Matrix, HS and DP in the AdWnt10b-treated group compared within AdGFP and normal P98 hair follicle controls (Red arrow, nuclear β-catenin; pink arrow, cytoplasm β-catenin; white arrow, membrane β-catenin). c. Statistical chart of Lef1, a downstream Wnt signaling target, was also markedly augmented in the Matrix and DP region, but not in the HS. d-e. Immunostaining and statistical chart reveals BrdU-labeled proliferating cells were increased in Wnt10b-induced enlarged hair follicles. f. Statistical graph showing β1-integrin expression was significantly increased in the HG, Bu and IFE regions of AdWnt10b-treated hair follicles. g. Ki67+ proliferating cells were located in the bulge, second hair germ and DP region 6d after the first AdWnt10 treatment. h. CD34 was unexpectedly localized to the hair shaft, especially in the ORS region. i. Double staining displayed colocalization of CD34 and BrdU both in the bulge and hair shaft of AdWnt10b-induced hair follicles but not in those of normal control hair follicles. Bu, bulge; HB, hair bulb; DP, dermal papilla; HS, hair shaft; HG, second hair germ; IFE, interfollicular epidermis; EB, epidermal basal layer. *P < 0.05.