Figure 2
Endothelial-specific Poldip2 knock-out abrogates inflammatory gene expression in LPS-induced lung injury. LPS injection induced a significant increase in expression of inflammatory markers [Tnfα (A), Iκbα (B)), chemoattractant molecules [Cxcl1 (C), Cxcl2 (D)], and the vascular activation marker [Vcam1 (E)] in Poldip2 EC+/+ mice. This effect was significantly blunted in Poldip2 EC−/− mice. Graphs represent averages ± SEM (n = 5). P < 0.0001, $$$P < 0.001, $$P < 0.01, compared to PBS injected Poldip2 EC+/+ mice, ##P < 0.01, #P < 0.05, compared to LPS injected Poldip2 EC+/+ mice (two-way ANOVA, with Tukey’s correction).

Endothelial-specific Poldip2 knock-out abrogates inflammatory gene expression in LPS-induced lung injury. LPS injection induced a significant increase in expression of inflammatory markers [Tnfα (A), Iκbα (B)), chemoattractant molecules [Cxcl1 (C), Cxcl2 (D)], and the vascular activation marker [Vcam1 (E)] in Poldip2 EC+/+ mice. This effect was significantly blunted in Poldip2 EC−/− mice. Graphs represent averages ± SEM (n = 5). P < 0.0001, $$$P < 0.001, $$P < 0.01, compared to PBS injected Poldip2 EC+/+ mice, ##P < 0.01, #P < 0.05, compared to LPS injected Poldip2 EC+/+ mice (two-way ANOVA, with Tukey’s correction).

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