Extended Data Fig. 7: Effects of Thy1 loss on various cell types during wounding.
From: THY1-mediated mechanisms converge to drive YAP activation in skin homeostasis and repair
a, Confocal images of the WT and Thy1-/- wound beds at 3 days post wound infliction (PWI) immunostained against T cell marker CD3. White dotted lines demarcate epidermis/dermis. b, Flow cytometry on wounds resected at day 3 PWI gated for CD45-APC+ cells (n = 3 pooled mice of each genotype). c,d., Immunoblots against NFκB p65 (c) and IκBα (d) in epidermal and dermal cells of WT and Thy1-/- telogenic (P56) dorsal skins. e, Dermis of adult WT and Thy1-/- mice after 7 days PWI stained for MCM2 and the dermal fibroblast marker PDGFRα. f., Percentage of proliferating papillary and reticular dermal cells. g,h, Immunostaining against Vimentin and Ki-67 (g), and CD31 and Ki-67 (h) in wound site dermis at day 3 PWI. i, Immunostaining against CD31 and Ki-67 in wound site dermis at 7 days PWI. j, Relative numbers of proliferating CD31+ cells at 3 and 7 days PWI in WT and Thy1-/- mice (n = 3 mice). All images and quantifications are representative of at least n = 3 mice of each genotype, unless otherwise indicated. Quantifications were performed on ≥ 60 fields of view ranging from 100-200μm. Western blots were performed on pooled proteins from n = 3 mice per genotype. Error bars indicate mean ± s.e.m. Scale bars, 50 μm (a,e,g,h,i).
