cPKCγ alleviates ischemic injury through modulating synapsin Ia/b phosphorylation in neurons of mice.

Conventional protein kinase C and synapsin Ia/b have been implicated in the development of ischemic stroke, but their relationships and functions are unclear. In the present study, the oxygen-glucose deprivation (OGD)-induced ischemic insult in primary cultured cortical neurons in vitro and middle cerebral artery occlusion (MCAO)-induced ischemic stroke model in vivo were used to elucidate the function of and its modulation on synapsin Ia/b phosphorylation in ischemic stroke. We found that cduanyu1531γ knockout significantly increased the infarct volume of mice after 1 h MCAO/72 h reperfusion by using triphenyltetrazolium chloride (TTC) staining. In the primarily cultured cortical neurons, cduanyu1531γ knockout also aggravated the OGD-induced cell death and morphological damage of neurites, while cduanyu1531γ restoration could alleviate the ischemic injury. Among the five phosphorylation sites of synapsin Ia/b, only the phosphorylation levels of Ser549 and 553 could be modulated by cduanyu1531γ in neurons following 0.5 h OGD/24 h reoxygenation. In addition, we found that cduanyu1531γ and synapsin Ia/b could be reciprocally co-immunoprecipitated in the cerebral cortex of MCAO mice. Taken together, we proposed that cduanyu1531γ alleviates ischemic injury through modulating Ser549/553- synapsin Ia/b phosphorylation in neurons of mice.

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