Fig. 2
From: Injury-activated glial cells promote wound healing of the adult skin in mice
Skin injury induces peripheral glial de-differentiation and proliferation. a p75 (green), MBP (red), and NF (white) triple immunolabelling of wound sections shows increased expression of the de-differentiation marker p75 and loss of the differentiation marker MBP as well as loss of NF in activated NBs. b, c Single-channel insets show expression of p75, MBP, and NF in activated and quiescent NBs in injured skin. d Quantification of NBs categorised based on NF labelling (NFHigh and NFlow) and p75 positivity (p75+ and p75−). e Immunolabelling of pERK (marker of activated MAPK signalling pathway) and Ki67 (marker for proliferative or cycling state) (red) in quiescent vs. activated NBs in injured skin. Activated NBs are characterised by p75 staining (green). f Quantification of Ki67+ nuclei in quiescent or activated NBs. g Double immunolabelling of p75 (green) and c-Jun (red) shows concomitant upregulation of both markers in activated vs. quiescent NBs in injured skin. Black arrowhead denotes a Ki67+ c-Jun− cell. White arrowheads denote Ki67+ c-Jun+ cells. h Quantification of proportion of proliferative (Ki67+) cells in c-Jun+ and c-Jun− fractions of de-differentiated (p75+) glial cells within NBs. Data are represented as mean ± SEM of N = 7 animals, n = 12 wounds for activated NBs and N = 5, n = 9 for quiescent NBs (d); 8 quiescent NBs from N = 2, n = 4 and 14 activated NBs from N = 4, n = 6 (f); N = 6, n = 7 (h). Scale bars, 100 µm. Wound samples are D7 post injury
