Induction of sialyl Lewis(X) on the surface of cultured rat vascular endothelial cells and cardiac myocytes by hypoxia/reoxygenation in vitro.

Neutrophils adhere to and roll on vascular endothelial cells (VECs) through interaction of selections and their carbohydrate ligands in the early stages of inflammation; this adhesion is then later strengthened through interaction of integrins on neutrophils with intercellular adhesion molecule-1 (ICAM-1) on endothelial cells. Recent, as yet unpublished studies showed that myocardial ischaemia/reperfusion caused rapid expression of sialyl Lewis(X) (SLe(X)), one of the carbohydrate ligands of selections, on VECs and cardiac myocytes and that an anti-SLe(X) monoclonal antibody (MAb) significantly reduced myocardial reperfusion injury in vivo, In the present study, to investigate whether or not ischaemia/reperfusion itself can induce the expression of SLe(X) on VECs and cardiac myocytes, the expression of SLe(X) on cultured rat VECs and cardiac myocytes was examined by treatment with hypoxia/reoxygenation in vitro, because ischaemia/ reperfusion stimuli may partly be due to hypoxia/reoxygenation. The expression of SLe(X) was induced rapidly and temporarily on the surface of cultured rat cardiac myocytes and VECs by hypoxia/reoxygenation in vitro. This strongly suggests that the expression of SLeX on the surface of myocardial cells is induced initially and directly by ischaemia/reperfusion, which results in the rolling attachment of neutrophils in the early stages of myocardial reperfusion injury.