Figure 1.

Injury Repair Is Delayed after Demethylase Inhibitor Application in Mouse Back Skin during Late Anagen/Catagen

(A) Scheme of cellular plasticity and methylation levels in quiescent and activated HFSCs.

(B) Scheme of demethylase inhibitor (DI) application and the punch wound experiment. A, Anagen; C, Catagen; T, Telogen; PD, postnatal day.

(C) Western blots for control vehicle (CT) or DI applied to wild-type mice during late Anagen/Catagen (PD35-42) phase and sacrificed at the ages indicated at top. For the whole blot, see Figure S1A.

(D) Quantification of the western blots in (B and S1A). Three mice were used per time point for statistical analysis. ^∗p = 0.005, ^∗∗p = 0.005, ^∗∗∗p = 0.009.

(E) Punch wound pictures of (PD35-42) CT- or DI-treated mice at different days after the punch wound.

(F) Punch wound size measurements on images like those in (E). N = 5 mice per group. ANOVA was used for significance test.

(G) Tenascin and K10 staining skin sections including the punch wound of wild-type mice after CT or DI application 1 week after the wound. Panels on the left are enlargements of corresponding white dotted line insets on the right.

(H) Blood vessel (CD31) and DNA (Hoechst) staining in 1-week punch wound skin sections of wild-type mice after CT or DI application. Arrows indicate the wound edges at the junction with normal skin.

(I) Fibroblast (vimentin) and K14 staining in 1-week punch wound skin sections of wild-type mice after CT or DI application. Arrows indicate the wound edges at the junction with normal skin.

Student’s t test was used for all significance tests except (F). All the experiments were executed twice. Scale bars, 20 μm.