PECAM-1在中性粒细胞与缺氧内皮细胞黏附中的作用。

Role of PECAM-1 in the adherence of PMN to hypoxic endothelial cells.

作者信息

Michiels C, Arnould T, Remacle J

机构信息

Laboratoire de Biochimie Cellulaire, Facultés Universitaires Notre Dame de la Paix, Namur, Belgium.

出版信息

Cell Adhes Commun. 1998 Jul;5(5):367-74. doi: 10.3109/15419069809010782.

DOI:10.3109/15419069809010782

PMID:9789684

Abstract

Hypoxia induces an increase in PMN adherence to endothelial cells for which an interaction between ICAM-1 and CD18/CD11b has been demonstrated. Since PECAM-1 has been shown to be involved in PMN transmigration through the endothelium and to increase the binding capacity of leukocyte CD18/CD11b, the role of this molecule in the hypoxia-induced PMN adherence was investigated. Hypoxia did not change the total surface expression of PECAM-1 on HUVEC and did not change the cell-cell border localization of this molecule as TNF-alpha did. In addition, blocking anti-PECAM-1 antibodies could not inhibit the increased adherence of unstimulated human PMN to hypoxia-incubated HUVEC while anti-ICAM-1 partially inhibited this process. These results indicate that PECAM-1 is probably not involved in the hypoxia-induced PMN adherence to endothelial cells.

摘要

缺氧会导致中性粒细胞（PMN）与内皮细胞的黏附增加，其中细胞间黏附分子-1（ICAM-1）与CD18/CD11b之间的相互作用已得到证实。由于血小板内皮细胞黏附分子-1（PECAM-1）已被证明参与PMN穿过内皮的迁移过程，并增加白细胞CD18/CD11b的结合能力，因此研究了该分子在缺氧诱导的PMN黏附中的作用。缺氧并未改变人脐静脉内皮细胞（HUVEC）上PECAM-1的总表面表达，也未像肿瘤坏死因子-α（TNF-α）那样改变该分子在细胞-细胞边界的定位。此外，阻断抗PECAM-1抗体不能抑制未刺激的人PMN对缺氧孵育的HUVEC增加的黏附，而抗ICAM-1可部分抑制这一过程。这些结果表明，PECAM-1可能不参与缺氧诱导的PMN与内皮细胞的黏附。