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

• Published in: ACTA HISTOCHEMICA ET CYTOCHEMICA Vol. 36; no. 4; pp. 385 - 391
• Main Authors: Ohtaki, Hirokazu, Endo, Sakura, Nakamachi, Tomoya, Yin, Li, Dohi, Kenji, Kudo, Yoshifumi, Iwai, Yumiko, Matsunaga, Masaji, Goto, Noboru, Shioda, Seiji
• Format: Journal Article
• Language: English
• Published: Sendai JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY 01-01-2003; Japan Science and Technology Agency
• Subjects: astrocytes; blood vessels; intercellular adhesion molecule-1 (ICAM-1); mice; transient focal ischemia
• ISSN: 0044-5991; 1347-5800
• DOI: 10.1267/ahc.36.385

Molecular mediators such as intercellular adhesion molecule-1 (ICAM-1) have been implicated in the induction of neuronal damage after ischemia/reperfusion. However, the time-dependent expression of ICAM-1 after transient ischemia and the relative influence of ICAM-1 on neuronal cell death are not well understood. We performed immunostaining for ICAM-1 and apoptotic-like neuronal cell death by in situ by terminal UTP-nucleotide 3'-OH-DNA end labeling (TUNEL) after a 1-hr transient middle cerebral artery occlusion (tMCAO) in mouse. ICAM-1-like immunoreactivity (ICAM-1-ir) was detected only to a slight extent in the brains of sham-operated control. ICAM-1-ir after tMCAO was noted in the ischemic region of the ipsilateral hemisphere within 3 to 6 hr, and increased significantly from 24 to 96 hr. The ICAM-1-ir was mainly localized in the endothelium of blood vessels, and was also observed in astrocytes 24 hr after tMCAO. While the endothelial expression of ICAM-1-ir overlapped with that of TUNEL staining, the astroglial expression of ICAM-1-ir was observed around the periphery of infarction, which did not recognize TUNEL-positive reaction. These results suggest that ICAM-1 expression in the mouse brain increases after tMCAO, and that the endothelial expression of ICAM-1 could be indicative of the induction of neuronal damage via leukocyte invasion.