Fig. 4: Chfr deletion in endothelial cells of mice suppresses LPS-induced vascular injury and mortality. | Nature Communications

Fig. 4: Chfr deletion in endothelial cells of mice suppresses LPS-induced vascular injury and mortality.

From: Ubiquitin ligase CHFR mediated degradation of VE-cadherin through ubiquitylation disrupts endothelial adherens junctions

Fig. 4

a Hematoxylin and eosin staining of lung sections from Chfrfl/fl and ChfrΔEC mice injected i.p. with LPS (10 mg/kg body weight) for 0, 6, and 24 h. Scale bar, 50 μm. Br, bronchus; V, vessel. b Protein contents, total cells, PMNs, and MPO activity in bronchoalveolar lavage fluid (BALF) from Chfrfl/fl and ChfrΔEC mice as in (a). c Lungs harvested at indicated time points after LPS i.p. (10 mg/kg body weight) were used for myeloperoxidase activity to assess PMN influx. d Chfrfl/fl and ChfrΔEC mice injected i.p. with LPS (10 mg/kg body weight) for 0, 6, and 24 h were used to assess lung vascular leak by measuring Evans blue bound albumin (EBA) uptake in lungs. b–d results shown are mean values ± SEM (n = 4 mice/genotype/group; two-way ANOVA followed by Tukey’s post-hoc test). e Survival of age- and weight-matched Chfrfl/fl and ChfrΔEC mice injected i.p. with LPS (10 mg/kg body weight). f Survival of age- and weight-matched Chfrfl/fl and ChfrΔEC mice challenged with CLP (e, f n = 8 mice/genotype; Chfrfl/fl vs ChfrΔEC; log-rank test).

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