Action of ERK5 in ischemic tolerance suggests its probable participation in the signaling mechanism

Abstract

Here we examined the effects of ischemia preconditioning and ketamine, an NMDA receptor antagonist, on the activation and its nucleus translocation of ERK5 in hippocampal CA1 region. Our results showed ERK5 was not activated in rat hippocampus CA1 region. But in cytosol extracts preconditioned with 3 min of sublethal ischaemia, ERK5 activation was enhanced significantly, with two peaks occurring at 3 hr and 3 days, respectively. This activation returned to base level 3 days later. The results lead us to conclude that preconditioning increased the activations of ERK5 during reperfusion after lethal ischemia through NMDA receptor. Preconditioning increased the activation and nucleus translocation of ERK5 during reperfusion after lethal ischemia through the NMDA receptor. These findings might provide some clues to understanding the mechanism underlying ischemia tolerance and to finding clinical therapies for stroke using the endogenous neuroprotection.

Keywords::

• ERK5
• Cerebral ischemia
• Ischemic tolerance
• NMDA receptor

Acknowledgments

This work was supported by three grants from the Great Research Project of the National Nature Science Foundation of China (NO. 90608015); Education Departmental Natural Science Research Funds of Jiangsu Province of China (NO. 08KJB180010); and Research Project of the National Youth Science Foundation of China (NO. 30700117).

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.