Figure 5
Figure 5. DV-elicited inflammasome activation depends on mitochondrial-derived ROS and RIP kinases. Platelets from healthy subjects were exposed to mock, infective DV-2 (DV), or heat-inactivated DV-2 (heat DV) in the presence or absence of the mitochondrial targeted antioxidant mitoTEMPO or the RIP1 inhibitor necrostatin-1 (Nec-1). Panels A and B show the fold changes for (A) MitoSox Red fluorescence and (B) caspase-1 activation related to mock values. (C-D) The levels of (C) IL-1β and (D) RANTES were determined in the supernatants of platelets incubated in each condition. The bars represent the mean ± SEM of 6 independent experiments using samples from different healthy donors. *P < .05 and **P < .01 compared with mock exposed platelets that were treated with the same drug. #P < .05 between DV-2–exposed platelets that were incubated with mitoTEMPO or Nec-1 and platelets that were incubated with DMSO. ND, not detected; ns, nonsignificant.

DV-elicited inflammasome activation depends on mitochondrial-derived ROS and RIP kinases. Platelets from healthy subjects were exposed to mock, infective DV-2 (DV), or heat-inactivated DV-2 (heat DV) in the presence or absence of the mitochondrial targeted antioxidant mitoTEMPO or the RIP1 inhibitor necrostatin-1 (Nec-1). Panels A and B show the fold changes for (A) MitoSox Red fluorescence and (B) caspase-1 activation related to mock values. (C-D) The levels of (C) IL-1β and (D) RANTES were determined in the supernatants of platelets incubated in each condition. The bars represent the mean ± SEM of 6 independent experiments using samples from different healthy donors. *P < .05 and **P < .01 compared with mock exposed platelets that were treated with the same drug. #P < .05 between DV-2–exposed platelets that were incubated with mitoTEMPO or Nec-1 and platelets that were incubated with DMSO. ND, not detected; ns, nonsignificant.

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