Figure 2: Increased susceptibility of the mg53−/− mice to overventilation and I/R-induced lung injury. | Nature Communications

Figure 2: Increased susceptibility of the mg53−/− mice to overventilation and I/R-induced lung injury.

From: Treatment of acute lung injury by targeting MG53-mediated cell membrane repair

Figure 2

(a) Haematoxylin and eosin staining of lung section derived from wild-type and mg53−/− mice under basal conditions. Mean linear intercept measurements (Lm) of alveolar spaces reveal significant difference between the wild-type and mg53−/− lung. (b) Representative images of wild-type and mg53−/− lung subjected to overventilation (upper panels). The subpleural lung images of wild-type and mg53−/− mice show PI+ alveolus cells after overventilation (lower panels). Scale bar, 10 μm. (c) Quantification of PI+ cells in the subplueral lung area after overventilation (n=4 for wild type; n=5 for mg53−/−, *P<0.05, Student’s t-test). (d). Survival rate of mg53−/− and wild-type mice was recorded after I/R. The product limit (Kaplan–Meier) estimate of the cumulative survival was assessed with the log-rank test to evaluate for significant differences in survival (*P<0.05, n=19 for mg53−/− mice and n=9 for wild type mice, Kaplan–Meier survival analysis (mean±s.e.m.). (e) Arterial blood samples were drawn from individual mice, the plasma PaO2 concentrations were measured (*P<0.05 versus wild type, n=6 in each group, analysis of variance (ANOVA), mean±s.e.m.). (f) Lung oedema was measured as the wet/dry weight ratio of the excised lung from mice (*P<0.05 versus wild type, n=5, ANOVA). Animals receiving normal low-tidal ventilation without I/R were used as sham controls.

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