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 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.
Soriano
S G
SG
Department of Anesthesia, Children's Hospital, Boston 02115, USA. soriano@a1.tch.harvard.edu
Wang
Y F
YF
Lipton
S A
SA
Dikkes
P
P
Gutierrez-Ramos
J C
JC
Hickey
P R
PR
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001710:Biotin; D002540:Cerebral Cortex / Q000098:blood supply* / Q000473:pathology; D053938:DNA Fragmentation; D003856:Deoxyuracil Nucleotides; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009336:Necrosis; D009474:Neurons / Q000737:chemistry / Q000166:cytology*; D019581:Neuropil / Q000473:pathology; D013194:Staining and Labeling
D003856:Deoxyuracil Nucleotides; D018799:Intercellular Adhesion Molecule-1; D001710:Biotin