Fig. 3 | Signal Transduction and Targeted Therapy

Fig. 3

From: TRIM47 is a novel endothelial activation factor that aggravates lipopolysaccharide-induced acute lung injury in mice via K63-linked ubiquitination of TRAF2

Fig. 3

TRIM47 deficiency reduces LPS-induced acute lung injury and pulmonary inflammation in mice. a Schematic strategy of generation of TRIM47 knockout mice. b Representative images of agarose gel electrophoresis for genotyping of TRIM47+/+, TRIM47+/−, and TRIM47−/− mice. c Representative images of the immunoblots of TIRM47 and β-actin in lungs from TRIM47+/+ and TRIM47−/− mice detected by western blot. d Pulmonary edema was represented as lung wet-to-dry ratio (n = 6, one-way ANOVA, **P < 0.01). e Survival rate of mice intraperitoneally administered with 15 mg/kg LPS (n = 16, the log-rank test, P < 0.01). f Representative images of the histological changes in lungs after LPS challenge examined by HE staining (n = 6). Scale bar, 100 μm. g The relative expression of TRIM47 and various pro-inflammatory cytokines in lungs was measured by real-time PCR (n = 6, one-way ANOVA, *P < 0.05, **P < 0.01). h The content of IL-1β, IL-6, and TNFα in the serum was detected by ELISA (n = 6, one-way ANOVA, *P < 0.05, **P < 0.01)

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