Seko Y, Enokawa Y, Tamatani T, Kannagi R, Yagita H, Okumura K, Yazaki Y
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
J Pathol. 1996 Nov;180(3):300-4. doi: 10.1002/(SICI)1096-9896(199611)180:3<300::AID-PATH650>3.0.CO;2-#.
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 Recent, as yet unpublished studies showed that myocardial ischaemia/reperfusion caused rapid expression of sialyl Lewis(X) (SLe(X)), one of the carbohydrate ligands of selections, on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.
在炎症早期，中性粒细胞通过选择素与其碳水化合物配体的相互作用，黏附于血管内皮细胞（VECs）并在其上滚动；随后，中性粒细胞上的整合素与内皮细胞上的细胞间黏附分子-1（ICAM-1）相互作用，使这种黏附作用得到加强。最近尚未发表的研究表明，心肌缺血/再灌注可使选择素的碳水化合物配体之一唾液酸化路易斯（X）（SLe（X））在VECs和心肌细胞上快速表达，且抗SLe（X）单克隆抗体（MAb）可在体内显著减轻心肌再灌注损伤。在本研究中，为探究缺血/再灌注本身是否能诱导VECs和心肌细胞上SLe（X）的表达，对培养的大鼠VECs和心肌细胞进行体外缺氧/复氧处理，检测SLe（X）的表达，因为缺血/再灌注刺激可能部分归因于缺氧/复氧。体外缺氧/复氧可使培养的大鼠心肌细胞和VECs表面迅速且短暂地诱导SLe（X）的表达。这有力地表明，心肌细胞表面的SLeX表达最初是由缺血/再灌注直接诱导的，这导致了心肌再灌注损伤早期中性粒细胞的滚动黏附。
