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. 2019 Jul 6;3:100009. doi: 10.1016/j.mbplus.2019.100009

Fig. 3.

Fig. 3

Loss of CCN1 impaired induction of collagen production and skin thickness in response to bleomycin-induced skin fibrosis. However, myofibroblasts differentiation still occurred in CCN1-deficient skin. A) An increase in CCN1 protein expression was observed in skin sections of wild-type mice subjected to bleomycin-induced skin fibrosis (p < 0.0001); CCN1−/− mice showed no CCN1 staining, as observed by staining with an anti-CCN1 antibody, as described in Methods. (Representative images shown; Graphs represent mean CCN1 positive cells +/− SD; one-way ANOVA; n = 5). B) Bleomycin-induced skin thickness (p = 0.0042) is not observed in CCN1−/− mice. Skin is significantly thinner in PBS CCN1−/− (p = 0.0175) and Bleomycin CCN1−/− (p = 0.0082) compared to PBS CCN1f/f. (Representative images shown; Graph shows mean skin thickness +/-SD; one-way ANOVA; n = 4). C) Trichrome images show CCN1−/− mice do not get an over-production of collagen in response to bleomycin induced fibrosis (p = 0.0228). (Representative images shown; Graph represents mean area collagen in images +/− SD; one-way ANOVA; n = 4). D) Birefringence analyses of picroSirius stained skin sections indicate that CCN1−/− does not display the excessive collagen fiber size and density seen in regular bleomycin-fibrosis. (Representative images shown; n = 6). E) Dermal increase in αSMA (p = 0.0037) seen in bleomycin-induced fibrosis is still observed in CCN1−/− dermis (p = 0.0071), compared to control PBS mice. (Representative images shown; Graphs represent mean αSMA positive cells +/− SD; one-way ANOVA; n = 5).