Increase in Surface Expression of ICAM-1, VCAM-1 and E-Selectin in Human Cerebromicrovascular Endothelial Cells Subjected to Ischemia-Like Insults

Publisher Website
Google Scholar
Abstract
Secondary ischemic brain injury has been shown to develop as a consequence of inflammation and vasogenic brain edema. In this study we show that inflammatory cytokines and simulated in vitro ischemia stimulate the surface expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial-leukocyte adhesion molecule-1 (E-selectin) in human cerebromicrovascular endothelial cells (HCEC) in culture. The levels of all three adhesion molecules were dramatically (3 to 10-fold) up-regulated by 4–24 hour exposure to the inflammatory cytokines, IL-1β (10–200 u/ml) or TNFα (50–200 u/ml), and by a 4 hour exposure to “simulated” in vitro ischemia, as determined by immunocytochemistry and ELISA. Following 24 hours of subsequent reperfusion, the expression of ICAM-1 and VCAM-1 was maintained at ischemia-induced levels, whereas E-selectin was no longer detectable. Both the cytokine- and ischemia-induced up-regulation of adhesion molecules were completely abolished by the transcriptional inhibitor, actinomycin D (10 µg/ml), and inhibited by the cycloxygenase (COX) inhibitor, indomethacin (300 µM). These findings implicate HCEC in the processes of leukocyte adhesion and recruitment in the brain durin stroke in vivo.

This publication has 11 references indexed in Scilit: