Action of ERK5 in ischemic tolerance suggests its probable participation in the signaling mechanism.
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.
Qi
Su-Hua
SH
School of Life Science and Biotechnology, China Pharmaceutical University, 24 Tongjia Street, Nanjing, PR China.
Guan
Qiu-Hua
QH
Wang
Min
M
Zhang
Guang-Yi
GY
D021581:Active Transport, Cell Nucleus / Q000502:physiology; D000818:Animals; D004789:Enzyme Activation; D018691:Excitatory Amino Acid Antagonists / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D019194:Ischemic Preconditioning; D007649:Ketamine / Q000378:metabolism*; D008297:Male; D048054:Mitogen-Activated Protein Kinase 7 / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000502:physiology*
D018691:Excitatory Amino Acid Antagonists; D007649:Ketamine; D048054:Mitogen-Activated Protein Kinase 7