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

Brain Res. 1998 Jan 12;780(2):337-41. doi: 10.1016/s0006-8993(97)01298-5.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Biotin
  • Cerebral Cortex / blood supply*
  • Cerebral Cortex / pathology
  • DNA Fragmentation
  • Deoxyuracil Nucleotides
  • Intercellular Adhesion Molecule-1 / metabolism*
  • Ischemic Attack, Transient / metabolism*
  • Male
  • Mice
  • Mice, Knockout
  • Necrosis
  • Neurons / chemistry
  • Neurons / cytology*
  • Neuropil / pathology
  • Staining and Labeling

Substances

  • Deoxyuracil Nucleotides
  • Intercellular Adhesion Molecule-1
  • Biotin