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Papers In Press, published online ahead of print March 29, 2005
J. Biol. Chem, 10.1074/jbc.M500003200
Submitted on January 1, 2005
Revised on March 29, 2005
Accepted on March 29, 2005

Neuroprotective effects of preconditioning ischemia on ischemic brain injury through down-regulating activation of JNK1/2 via N-methyl-D-aspartate (NMDA) receptor mediated Akt1 activation

Bei Miao, Xiaohui Yin, Dongsheng Pei, Quanguang Zhang, and Guang-Yi Zhang

Department of Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002

Corresponding Author: gyzhang{at}xzmc.edu.cn

Our previous studies have demonstrated that JNK (c-Jun N-terminal kinase) signaling pathway plays an important role in ischemic brain injury and is mediated via GluR6 (Glutamate receptor 6). Others studies have shown that NMDA receptor is involved in the neuroprotection of ischemic preconditioning. Here, we examined whether ischemic preconditioning downregulates activation of MLK (Mixed-lineage kinase)-JNK signaling pathway via NMDA receptor mediated Akt1 activation. In our present results, ischemic preconditioning could not only inhibit activations of MLK3, JNK1/2 and c-Jun, but also enhance activation of Akt1. In addition, both NMDA (an agonist of NMDA receptor) and preconditioning showed neuroprotective roles. In contrast, ketamine, an antagonist of NMDA receptor,prevented the above effects of preconditioning. Further studies indicated that LY294002, an inhibitor of PI-3K (phosphoinositide 3-kinase) which is an upstream signaling proteins of Akt1, could block neuroprotection of preconditioning, and KN62, an inhibitor of CaM-K (calmodulin-dependent protein kinase) kinase, also achieved the same effects as LY294002. Therefore, both PI-3K and CaM-K are involved in the activation of Akt1 in ischemic tolerance. Taken together, our results indicate that preconditioning can inhibit activation of JNK signaling pathway via NMDA receptor mediated Akt1 activation and induce neuroprotection in hippocampal CA1 region.


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