ICAM-1 dependent pathway is not involved in the development of neuronal apoptosis after transient focal cerebral ischemia

We examined brain sections from ICAM-1 deficient mice (−/−) and their nontransgenic littermates (+/+) after focal cerebral ischemia and reperfusion (I/R) for the presence of apoptosis. Despite the reduction in necrosis, the −/− mice had apoptotic cells in the ischemic hemisphere as shown by terminal...

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Bibliographic Details
Published in:Brain research 1998-01, Vol.780 (2), p.337-341
Main Authors: Soriano, Sulpicio G, Wang, Yanming F, Lipton, Stuart A, Dikkes, Pieter, Gutierrez-Ramos, Jose-Carlos, Hickey, Paul R
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - physiology
Biological and medical sciences
Biotin
Cerebral Cortex - blood supply
Cerebral Cortex - pathology
Cerebral ischemia
Deoxyuracil Nucleotides
DNA Fragmentation
ICAM-1
Intercellular Adhesion Molecule-1 - metabolism
Ischemic Attack, Transient - metabolism
Male
Medical sciences
Mice
Mice, Knockout
Necrosis
Neurology
Neurons - chemistry
Neurons - cytology
Neuropil - pathology
Staining and Labeling
Vascular diseases and vascular malformations of the nervous system
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Summary:We examined brain sections from ICAM-1 deficient mice (−/−) and their nontransgenic littermates (+/+) after focal cerebral ischemia and reperfusion (I/R) for the presence of apoptosis. Despite the reduction in necrosis, the −/− mice had apoptotic cells in the ischemic hemisphere as shown by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining and DNA laddering. ICAM-1 deficiency minimizes necrosis but not apoptosis after temporary MCAO in mice, thereby leaving the potential for delayed neuronal cell death despite ICAM-1 inactivation.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(97)01298-5