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KMID : 0811720050090000059
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Korean Journal of Physiology & Pharmacology
2005 Volume.9 No. 0 p.59 ~ p.0
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Mild Hypothermia Inhibits ICAM-1 Expression via a Enhanced ERK1/2 Activity in Experimental Stroke
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Choi Jung-Sook
Han Hyung-Soo
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Abstract
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Mild hypothermia has been shown to be neuroprotective in focal ischemia. We previously observed expression of Intercellular adhesion molecule-1 (ICAM-1) was decreased by hypothermia and identified extracellular signal regulated kinase1/2 (ERK1/2) activation was increased in the endothelium during the early stage of hypothermic ischemia. In the present study, we explored the protective mechanism of ERK1/2 in ischemic injury using a MEK1/2 inhibitor, U0126, in vivo and in vitro. Rats were subjected to 2 hours of middle cerebral artery occlusion followed by 22 hours of reperfusion under room temperature (37oC) or hypothermia (33oC). Endothelial cells were exposed to oxygen glucose deprivation (OGD) and reperfusion. U0126 was administered 30 minutes before the onset of ischemia. Elk-1 and c-Fos were not observed in the endothelium but signal transducer and activator of transcription 3 (STAT3) was increased by the ischemic insult and attenuated by hypothermia. Inhibition of ERK1/2 activation affected STAT3 activation. Treatment with U0126 markedly increased ICAM-1 expression in hypothermia. From these data, we suggest that hypothermic attenuation of ICAM expression is mediated by enhanced activation of ERK1/2 and attenuated STAT3 activation.
Source: Korean Journal of Physiology & Pharmacology.2005 Oct;9(Suppl I):S84-S84
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KEYWORD
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Hypothermia, ERK1/2, ICAM-1
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