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Bing-Mei Zhu, Yuko Ishida, Gertraud W

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1 SOCS3 Negatively Regulates the gp130–STAT3 Pathway in Mouse Skin Wound Healing 
Bing-Mei Zhu, Yuko Ishida, Gertraud W. Robinson, Margit Pacher-Zavisin, Akihiko Yoshimura, Philip M. Murphy, Lothar Hennighausen  Journal of Investigative Dermatology  Volume 128, Issue 7, Pages (July 2008) DOI: /sj.jid Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

2 Figure 1 Macroscopic changes at skin excisional wound sites. (a) Wound sites were photographed at the indicated time. Day 0 (d0) pictures were taken immediately after the injury. Representative results from 12 individual mice in each group are shown. (b) Changes in percentage of wound area at each time point compared with the original wound area. (c) Hydroxyproline content, an index of collagen accumulation at the wound site. Values represent mean±SEM. *P<0.05, **P<0.01 compared with control mice. Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

3 Figure 2 Wound healing in the absence of SOCS3 and gp130. (a) Histopathological analyses of epidermis at skin wound sites of control, Socs3fl/fl; MMTV-Cre, Socs3fl/fl; K5, and Socs3fl/fl; MMTV-Cre; gp130fl/fl; MMTV-Cre mice at days 6 (upper panel) and 14 (lower panel) after injury. Paraffin sections were stained with hematoxylin and eosin. Rectangles indicate epidermis; * indicates hair follicles. (b) Immunohistochemical staining for proliferating-cell nuclear antigen (red) and K5 (green) at the wound sites of control, Socs3fl/fl; MMTV-Cre, Socs3fl/fl; K5, and Socs3fl/fl; MMTV-Cre; gp130fl/fl; MMTV-Cre mice at days 6 (upper panel) and 10 (lower panel) after injury. # Indicates epidermis. Bar=100μm. Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

4 Figure 3 Activation of STATs in wound healing. Immunohistochemical staining for phosphorylated STAT3 (a) and phosphorylated STAT5 (b) at wound sites in control, Socs3fl/fl; MMTV-Cre, Socs3fl/fl; K5, and Socs3fl/fl; MMTV-Cre; gp130fl/fl; MMTV-Cre mice at days 0 (upper panel), 6 (middle panel), and 14 (lower panel). Representative results from six mice in each group are shown. Red, P-STATs; green, E-cadherin. * Indicates hair follicles; # indicates epidermis. Bar=100μm. For color figure see online version. Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

5 Figure 4 Recruitment of immune cells. Immunohistochemical analyses of neutrophil (a–d) and macrophage (g–j) recruitment at skin excisional wound sites. Anti-MPO on day 3 (a–d) or anti-F4/80 on day 6 (g–j) was used for immunohistochemical staining for neutrophils and macrophages, respectively. Hematoxylin was used for counterstaining. Arrows indicate positively stained cells. Representative results from three independent experiments are shown. (e) MPO activity at the wound site was determined to evaluate neutrophil accumulation. (f) Number of circulating neutrophils in peripheral blood in the different groups of mice. (k) Number of macrophages per microscopic field. All values represent the mean±SEM (n=6 mice). *P<0.05, compared with control mice. Bar=50μm. Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

6 Figure 5 Model depicting the consequences of absence of SOCS3 in wound healing. (a) Diagram of the IL-6–gp130–STAT3 signaling pathway and the molecular consequences arising upon loss of Socs3. P, phosphorylated tyrosine residues; GAS, STAT-binding site. (b) Hyperproliferation of keratinocytes and increased IL-6 and chemokines and elevated filtration of inflammatory cells at wound sites upon the deletion of SOCS3 in skin. KC, keratinocyte-derived chemokine; MIP, macrophage-inflammatory protein. Journal of Investigative Dermatology  , DOI: ( /sj.jid ) Copyright © 2008 The Society for Investigative Dermatology, Inc Terms and Conditions

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