Genetic inhibition of PKCε attenuates neurodegeneration after global cerebral ischemia in male mice.

Global cerebral ischemia that accompanies cardiac arrest is a major cause of morbidity and mortality. C epsilon is a member of the novel subfamily and plays a vital role in ischemic preconditioning. Pharmacological activation of before cerebral ischemia confers neuroprotection. The role of endogenous duanyu1531ε after cerebral ischemia remains elusive. Here we used male mice to assess the effects of duanyu1531ε deficiency on neurodegeneration after transient global cerebral ischemia (tGCI). We found that the cerebral vasculature, blood flow, and the expression of other duanyu1531 isozymes were not altered in the duanyu1531ε-null mice. Spatial learning and memory was impaired after tGCI, but the impairment was attenuated in male duanyu1531ε-null mice as compared to male wild-type controls. A significant reduction in Fluoro-Jade C labeling and mitochondrial release of cytochrome C in the hippocampus was found in male duanyu1531ε-null mice after tGCI. Male duanyu1531ε-null mice expressed increased levels of in the mitochondria, which may prevent the translocation of duanyu1531δ from the cytosol to the mitochondria after tGCI. Our results demonstrate the neuroprotective effects of duanyu1531ε deficiency on neurodegeneration after tGCI, and suggest that reduced mitochondrial translocation of duanyu1531δ may contribute to the neuroprotective action in male duanyu1531ε-null mice.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}