scholarly journals Increased Expression of Intercellular Adhesion Molecule-1 (ICAM-1) in Mouse Brain Following Transient Cerebral Ischemia

2003 ◽  
Vol 36 (4) ◽  
pp. 385-391 ◽  
Author(s):  
Hirokazu Ohtaki ◽  
Sakura Endo ◽  
Tomoya Nakamachi ◽  
Li Yin ◽  
Kenji Dohi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Mouse Brain ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Transient Cerebral Ischemia ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

scholarly journals The Protective Effects of Preconditioning on Cerebral Endothelial Cells in Vitro

2003 ◽  
Vol 23 (11) ◽  
pp. 1348-1355 ◽  
Author(s):  
Anuska V Andjelkovic ◽  
Svetlana M Stamatovic ◽  
Richard F Keep
Keyword(s):  
Endothelial Cells ◽  
Lactate Dehydrogenase ◽  
Mouse Brain ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Cerebral Endothelial Cells ◽  
Lactate Dehydrogenase Release

Ischemic preconditioning (PC) can markedly reduce ensuing ischemic damage. Although most attention has focused on the neuronal effects of PC, the authors have recently shown that ischemic PC reduces ischemia-induced cerebrovascular damage. In vivo, it is difficult to ascertain whether this is a direct cerebrovascular effect of PC. This study, therefore, examined whether cerebral endothelial cells can be preconditioned in vitro in the absence of other cell types. Experiments were performed on an immortalized mouse brain endothelial cell line or primary cultures of mouse brain microvessel endothelial cells. Cells were exposed to oxygen glucose deprivation (OGD) of either short duration, as a PC stimulus, or a long duration (5 hours) with or without reoxygenation to induce endothelial damage. Endothelial injury was assessed by measuring lactate dehydrogenase release and the expression of intercellular adhesion molecule-1 at the protein and mRNA levels. Experiments indicated that 1 hour of OGD was the optimal PC stimuli and that a 1 or 3 day interval was the optimal time interval between the PC stimulus and the injurious event. Preconditioned cells had less lactate dehydrogenase release during OGD (± reoxygenation) and reduced intercellular adhesion molecule-1 expression after OGD with reoxygenation. This study shows that cerebral endothelial cells can be directly preconditioned. The importance of this phenomenon in the overall effects of PC on the brain remains to be elucidated. Understanding the protective mechanisms elicited by PC may give insight into how to prevent ischemia-induced vascular damage (e.g., hemorrhagic transformation).

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

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Jung Sook Choi ◽  
Jaechan Park ◽  
Kyoungho Suk ◽  
Cheil Moon ◽  
Yong-Ki Park ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Adhesion Molecule ◽  
Vascular Endothelium ◽  
Focal Cerebral Ischemia ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Hypothermic Condition

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.

Control of islet intercellular adhesion molecule-1 expression by interferon-alpha and hypoxia

Diabetes ◽  
1996 ◽  
Vol 45 (10) ◽  
pp. 1336-1343 ◽  
Author(s):  
D. Chakrabarti ◽  
X. Huang ◽  
J. Beck ◽  
J. Henrich ◽  
N. McFarland ◽  
...  
Keyword(s):  
Interferon Alpha ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1
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