The role of CDK5 activation in neuronal death and angiogenesis after ischemic stroke

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The aim of this study was to clarify the role of Cdk 5 activation in neuronal death and angiogenesis in the brain after transient focal cerebral ischemia (tFCI). After reperfusion, both Cdk5 activation and p25/p35 expression were significantly increased at 6 h compared with the control and decreased the expression at 3 days and recovererd at 7 days as detected by immunoblotting. p25/p35 was significantly upregulated in neurons in the ischemic area at 1 day and also upregulated in microvessels in the ischemic boundary zone from 3 to 7 days after reperfusion. Changes in BBB leakage indicated that BBB breakdown significantly increased 3 days after reperfusion. These findings suggest that Cdk 5 may be related to not only neuronal death but also angiogenesis after tFCI and can be a target for antiangiogenic therapy.