Premium
INDUCTION OF SIALYL LEWIS X ON THE SURFACE OF CULTURED RAT VASCULAR ENDOTHELIAL CELLS AND CARDIAC MYOCYTES BY HYPOXIA/REOXYGENATION IN VITRO
Author(s) -
SEKO YOSHINORI,
ENOKAWA YOSHIFUMI,
TAMATANI TAKUYA,
KANNAGI REIJI,
YAGITA HIDEO,
OKUMURA KO,
YAZAKI YOSHIO
Publication year - 1996
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199611)180:3<300::aid-path650>3.0.co;2-#
Subject(s) - myocyte , hypoxia (environmental) , ischemia , in vitro , reperfusion injury , in vivo , monoclonal antibody , inflammation , intracellular , cell adhesion molecule , antibody , chemistry , immunology , microbiology and biotechnology , medicine , biology , biochemistry , oxygen , organic chemistry
Neutrophils adhere to and roll on vascular endothelial cells (VECs) through interaction of selectins 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 Recent, as yet unpublished studies showed that myocardial ischaemia/reperfusion caused rapid expression of sialyl Lewis X (SLe X ), one of the carbohydrate ligands of selectins, on VECs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 SLe X 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.