Does caspase-3 contribute to ZO-1 and Cl-5 tight-junction disruption in rapid anoxic neurovascular unit damage?
Our data provide evidence that caspase-3 is rapidly activated during acute cerebral ischemia predominantly without triggering DNA-fragmentation in BEC. Further we detected fast TJ protein disruptions which could be partly blocked by caspase-3 inhibition with Z-DEVD-fmk. We suggest that the basis for clinically relevant BBB breakdown in form of TJ disruptions is initiated within minutes during ischemia and that caspase-3 contributes to this process.
pEHG inhibits flux at the G2/M transition, but has no effect on cell death.