Cited by 185Acute Ischemic Stroke ManagementNeuroinflammation and Neurodegeneration MechanismsCell Adhesion Molecules Research

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Antibodies against Adhesion Molecules Reduce Apoptosis after Transient Middle Cerebral Artery Occlusion in Rat Brain

Chopp, Michael, Li, Yi, Jiang, Ning, Zhang, Rui Lan, Prostak, Jonathan·1996·Journal of Cerebral Blood Flow & Metabolism

DOI 10.1097/00004647-199607000-00007

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Abstract

We tested the hypothesis that treatment of transient focal cerebral ischemia in rat with antibodies directed against adhesion molecules reduces apoptosis. Rats (n = 31) were subjected to 2 h of middle cerebral artery (MCA) occlusion induced by intraluminal insertion of a nylon monofilament into the internal carotid artery. Upon reperfusion, animals were treated with monoclonal antibodies directed against intercellular adhesion molecule (ICAM)-1) (n = 8) or integrin CD11b/CD18 (n = 10), or administered IgG1 as a control (n = 13). At 48 h after ischemia, animals were killed and the brains analyzed for ischemic cell damage, using hematoxylin and eosin (H/E); apoptosis, using the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) method; and inflammatory cells, using immunohistochemistry with an anti-myeloperoxidase (MPO) antibody. Data revealed a significant reduction in the volume of infarction (p < 0.01) and a decline in the absolute (p < 0.001), and normalized (to the ischemic areas, p < 0.05) numbers of apoptotic cells in both animals treated with anti-ICAM-1 and anti-CD11b antibodies compared to control animals. The numbers of immunoreactive MPO cells were also reduced in the treatment groups compared to those in the control group (p < 0.05). These data suggest that treatment with anti-adhesion molecule antibodies selectively reduce apoptosis, and that a contributing factor to the beneficial effect of antibody treatment for reducing ischemic cell damage may be a reduction in numbers of apoptotic cells.

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Authors: Chopp, M., Li, Y., Jiang, N., Zhang, R. L., & Prostak, J.
Affiliations: Henry Ford Health (US)
ORCID: Chopp, Michael
Li, Yi
Jiang, Ning
Prostak, Jonathan
Venue: Journal of Cerebral Blood Flow & Metabolism
Publisher: SAGE Publications
Published: 1996-07
Volume: 16
Issue: 4
Pages: 578-584
ISSN: 0271-678X (ISSN-L)
1559-7016
DOI: 10.1097/00004647-199607000-00007
OpenAlex: W2056824541
Cited by: 185
References: 76
Citations by year: 2025: 1 · 2022: 3 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 4 · 2017: 3 · 2016: 2 · 2015: 3 · 2014: 6 · 2013: 6 · 2012: 3
FWCI: 13.52
Type: journal article
Language: en
Open access: closed
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations: Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
PubMed (publishedVersion)
Funders: Hort Innovation
National Institutes of Health (5r01ns034184-04, 5r01ns033627-08)
National Institute of Neurological Disorders and Stroke (R01NS-33627, P01NS023393, R01NS-34184)
Topics: Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
Keywords: adhesion molecules, apoptosis, transient middle cerebral artery occlusion, focal cerebral ischemia, ICAM-1, CD11b/CD18 integrin, infarct size, ischemia-reperfusion injury, neuroprotection
MeSH terms: Animals, Antibodies, Monoclonal, Arterial Occlusive Diseases, Brain, Cell Count, Cerebrovascular Disorders, Male, Peroxidase, Cell Adhesion Molecules, Macrophage-1 Antigen, Apoptosis, Rats

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Antibodies against Adhesion Molecules Reduce Apoptosis after Transient Middle Cerebral Artery Occlusion in Rat Brain

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