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. Author manuscript; available in PMC: 2015 Oct 1.
Published in final edited form as: Circ Cardiovasc Genet. 2014 Jul 21;7(5):615–624. doi: 10.1161/CIRCGENETICS.113.000398

Figure 8.

Figure 8

Platelet TLR4 is necessary and sufficient for the induction of platelet dysfunction and organ injury in HS-R. Wild-type (LOXP) and mice lacking TLR4 on platelets (PF4-cre) were depleted of their platelets using anti-CD41 antibody and subsequently transfused donor platelets isolated from either their littermates (LOXPtransLOXP, PF4-cretransPF4-cre) as controls or from donors with opposite TLR4 status with respect to their platelets (LOXPtransPF4-cre, PF4-cretransLOXP) to test the specific role of TLR4 on platelets in HS-R. (A) TEGs pre and post HS-R are shown and the MA are quantified in (B) as means ± SEM (n = 5 mice/group). (C) rSerum AST levels including both sham and HS-R (means ± SEM (n = 5 mice/group)). *p<0.01 vs. control. #p<0.05 vs. HS-R group of LOXPtransLOXP mice.