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. Author manuscript; available in PMC: 2013 Jun 1.
Published in final edited form as: Kidney Int. 2012 Aug 15;82(11):1195–1207. doi: 10.1038/ki.2012.268

Figure 7.

Figure 7

Conditional endothelial knockout of MyD88 decreases PTX3 production and endothelial activation. Renal pedicles of “Wildtype” [MyD88f/f; Tie2Cre(−)] and “conditional MyD88 KO” [MyD88f/f; Tie2Cre(+)] mice were clamped for 23min. (A) Kidney PTX3 was measured by ELISA at baseline, 4hr, and 18hr reperfusion. The right kidney was harvested as control. (B) Plasma PTX3 was measured by ELISA at the same time points. In both “A” and “B”, the error bars stand for mean±SEM, n=3 per group. The 4 groups at each time point were analyzed by one-way ANOVA, and then pairwise comparisons made by the Holm-Sidak method. *P < 0.05 IRI versus sham, §P < 0.05 IRI MyD88f/f; Tie2Cre(−) versus MyD88f/f, Tie2Cre(+) at 18hr reperfusion; NS: not significant. (C) Endothelial markers were detected by qRT-PCR on CD31+ cells isolated from kidneys at 4hr reperfusion. Data were analyzed by the comparative Ct method. The calibrator gene is gene of interest taken from the sham kidney. Error bars stand for mean±SEM, n=3 per group, §P < 0.05 MyD88f/f; Tie2Cre(−) IRI versus sham,*P < 0.05 MyD88f/f; Tie2Cre(+) IRI versus sham.