Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model

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...

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Main Authors: Jung Sook Choi, Jaechan Park, Kyoungho Suk, Cheil Moon, Yong-Ki Park, Hyung Soo Han
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:Stroke Research and Treatment
Online Access:http://dx.doi.org/10.4061/2011/846716
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author Jung Sook Choi
Jaechan Park
Kyoungho Suk
Cheil Moon
Yong-Ki Park
Hyung Soo Han
author_facet Jung Sook Choi
Jaechan Park
Kyoungho Suk
Cheil Moon
Yong-Ki Park
Hyung Soo Han
author_sort Jung Sook Choi
collection DOAJ
description 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.
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spelling doaj-art-cce6cbf495b5410a996887c3da7a1a2e2025-08-20T03:19:32ZengWileyStroke Research and Treatment2042-00562011-01-01201110.4061/2011/846716846716Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia ModelJung Sook Choi0Jaechan Park1Kyoungho Suk2Cheil Moon3Yong-Ki Park4Hyung Soo Han5Department of Physiology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, 101 Dongin 2 Ga, Jung Gu, Daegu 700-422, Republic of KoreaDepartment of Neurosurgery, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, 101 Dongin 2 Ga, Jung Gu, Daegu 700-422, Republic of KoreaDepartment of Pharmacology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, 101 Dongin 2 Ga, Jung Gu, Daegu 700-422, Republic of KoreaDepartment of Brain Science, Daegu Gyeongbuk Institute of Science and Technology, Daegu 704-948, Republic of KoreaDepartment of Herbology, Dongguk University College of Oriental Medicine, Gyeong Ju 780-714, Republic of KoreaDepartment of Physiology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, 101 Dongin 2 Ga, Jung Gu, Daegu 700-422, Republic of KoreaIntercellular 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.http://dx.doi.org/10.4061/2011/846716
spellingShingle Jung Sook Choi
Jaechan Park
Kyoungho Suk
Cheil Moon
Yong-Ki Park
Hyung Soo Han
Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model
Stroke Research and Treatment
title Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model
title_full Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model
title_fullStr Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model
title_full_unstemmed Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model
title_short Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model
title_sort mild hypothermia attenuates intercellular adhesion molecule 1 induction via activation of extracellular signal regulated kinase 1 2 in a focal cerebral ischemia model
url http://dx.doi.org/10.4061/2011/846716
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