The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury

ZHOU Beiqun; ZHU Jiangtao

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The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury

ZHOU Beiqun #,ZHU Jiangtao *

The Second Affiliated Hospital of Soochow University,Suzhou,215004

*Correspondence author

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Funding: National Natural Science Foundation of China （No.813111078）

Opened online:24 May 2016

Accepted by: none

Citation: ZHOU Beiqun,ZHU Jiangtao.The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury[OL]. [24 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4690231

Mixed lineage kinase domain-like protein (MLKL) was recently identified to play a critical role in necrotic cell death. To examine its role in ischemia injury, we examined its expression and the degradation of MLKL on neuroprotective effects in a middle cerebral artery occlusion (MCAO) model. We found that MLKL expression was significantly increased at 6 h after reperfusion and reached peak at 48 h after I/R injury. Our findings further demonstrated that a small chemical Necrosulfonamide (NSA) decreased MLKL level after I/R injury by increasing the degradation of MLKL through the ubiquitination proteasome pathway. The degradation of MLKL by NSA also increased cleaved PARP-1 level, a marker of apoptosis. The reduction of MLKL by NSA markedly improved neurological deficits compared with vehicle-treated mice after MCAO. NSA pre-treatment and post-treatment reduced infarct volume even when NSA was administrated at 4 h after I/R injury, indicating a long therapeutic window of NSA treatment. These findings suggest that MLKL plays a critical role in ischemic injury and is a new therapeutic target for stroke. Therefore, Promoting the degradation of MLKL may represent a novel avenue for reducing necrotic cell death after ischemic brain injury.

Keywords:Necrosulfonamide; MLKL; ischemia reperfusion injury; necrosis

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