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. 2021 May 20;16(6):1568–1583. doi: 10.1016/j.stemcr.2021.04.015

Figure 2.

Figure 2

PBMT drives HFSC activation by inhibiting β-CATENIN degradation

(A and B) Western blot (A) and immunofluorescence (B) analysis of β-CATENIN levels after continuous PBMT treatment in mouse HF for 4 days, n = 8 mice per group and >60 HFs per mouse. ANOVA was used for significance test. ∗p < 0.05.

(C) Telogen-anagen transition analysis in β-Catenin gene knockout after PBMT, n = 6 mice.

(D) H&E images of the dorsal skin of mice after PBMT on days 14, n = 6 mice per group and >20 sections. ANOVA was used for significance test. ∗∗∗p < 0.001.

(E) Flow cytometry detected the proliferation of HFSCs on the 14th day of PBMT, n = 6 mice per group and >60 HFs per mouse. ANOVA was used for significance test. ∗∗∗p < 0.001.

(F) Immunofluorescence and flow cytometry were used to detect whether SOX9 and K15 in HFSCs were positive.

(G) The β-CATENIN protein level in mouse HFSCs was analyzed by western blot at different times after PBMT. The data represent mean ± SD, n = 3 independent replicates. ∗p < 0.05; ∗∗∗p < 0.001.

(H) Representative western blot of HFSCs treated with PBMT for 2 h and then incubated with or without MG132 for 6 h. The data represent mean ± SD, n = 3 independent replicates. ∗∗∗p < 0.001.