Figure 4
Figure 4. Blockade of endothelial NF-κB signaling reversed LPS-induced EPCR down-regulation. (A-C) Western blot photographs showing levels of EPCR protein in heart (A), kidney (B), and liver (C) of WT-Con (WT-C), WT-LPS (WT-L), TG-Con (TG-C), and TG-LPS (TG-L) mice at 6 hours after saline or LPS injection. Actin indicates membrane for EPCR blotting was reblotted with actin antibody. (D) Densitometry quantification of EPCR bands. Tissue levels of EPCR protein were comparable in all 3 organs between WT-Con and TG-Con mice and were greatly reduced in these organs of WT-LPS mice. Reduction in tissue levels of EPCR protein was not observed in these organs of TG-LPS mice. Data are mean ± SEM of 6 to 8 mice. *P < .001, compared with any other group. #P < .01, compared with the WT-LPS group.

Blockade of endothelial NF-κB signaling reversed LPS-induced EPCR down-regulation. (A-C) Western blot photographs showing levels of EPCR protein in heart (A), kidney (B), and liver (C) of WT-Con (WT-C), WT-LPS (WT-L), TG-Con (TG-C), and TG-LPS (TG-L) mice at 6 hours after saline or LPS injection. Actin indicates membrane for EPCR blotting was reblotted with actin antibody. (D) Densitometry quantification of EPCR bands. Tissue levels of EPCR protein were comparable in all 3 organs between WT-Con and TG-Con mice and were greatly reduced in these organs of WT-LPS mice. Reduction in tissue levels of EPCR protein was not observed in these organs of TG-LPS mice. Data are mean ± SEM of 6 to 8 mice. *P < .001, compared with any other group. #P < .01, compared with the WT-LPS group.

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