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Mild hypothermia attenuates intercellular adhesion molecule-1 induction via activation of extracellular signal-regulated kinase-1/2 in a focal cerebral ischemia model

Title
Mild hypothermia attenuates intercellular adhesion molecule-1 induction via activation of extracellular signal-regulated kinase-1/2 in a focal cerebral ischemia model
Authors
Han, H.S.[Han, Hyung Soo]Choi, J.S.[ Choi, Jung Sook]Park, J.[ Park, Jaechan]Suk, K.[ Suk, Kyoungho]Moon, C.[Moon, Cheil]Park, Y.-K.[Park, Yong-Ki]
DGIST Authors
Moon, C.[Moon, Cheil]
Issue Date
2011
Citation
Stroke Research and Treatment
Type
Article
Article Type
Article
Keywords
Animal CellAnimal ExperimentAnimal ModelBrain Blood VesselBrain IschemiaControlled StudyEnzyme ActivationInduced HypothermiaIntercellular Adhesion Molecule-1MaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MouseNon-HumanPriority JournalProtein InductionProtein PhosphorylationRatSTAT3 ProteinTherapy EffectVascular Endothelium
ISSN
2090-8105
Abstract
Intercellular adhesion molecule-1 (ICAM-1) in cerebral vascular endothelium induced by ischemic insult triggers leukocyte infiltration and inflammatory reaction. We investigated the mechanism of hypothermic suppression of ICAM-1 in a model of focal cerebral ischemia. Rats underwent 2 hours of middle cerebral artery occlusion and were kept at 37()C or 33()C during occlusion and rewarmed to normal temperature immediately after reperfusion. Under hypothermic condition, robust activation of extracellular signal-regulated kinase-1/2 (ERK1/2) was observed in vascular endothelium of ischemic brain. Hypothermic suppression of ICAM-1 was reversed by ERK1/2 inhibition. Phosphorylation of signal transducer and activator of transcription 3 (STAT3) in ischemic vessel was attenuated by hypothermia. STAT3 inhibitor suppressed ICAM-1 production induced by stroke. ERK1/2 inhibition enhanced phosphorylation and DNA binding activity of STAT3 in hypothermic condition. In this study, we demonstrated that hypothermic suppression of ICAM-1 induction is mediated by enhanced ERK1/2 activation and subsequent attenuation of STAT3 action. Copyright ? 2011 Jung Sook Choi et al.
URI
http://hdl.handle.net/20.500.11750/3480
DOI
10.4061/2011/846716
Publisher
Hindawi Publishing Corporation
Related Researcher
Files:
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Collection:
Brain and Cognitive SciencesETC1. Journal Articles


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