PECAM-1在PMN粘附于缺氧内皮细胞中的作用。

C Michiels, T Arnould, J Remacle
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引用次数: 13

摘要

缺氧诱导PMN粘附内皮细胞的增加,ICAM-1和CD18/CD11b之间的相互作用已被证实。由于PECAM-1已被证明参与PMN通过内皮的转运,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粘附中的作用。缺氧没有改变PECAM-1在HUVEC表面的总表达,也没有像tnf - α那样改变该分子的细胞-细胞边界定位。此外,阻断抗pecam -1抗体不能抑制未刺激的人PMN对缺氧培养的HUVEC的粘附性增加,而抗icam -1则部分抑制了这一过程。这些结果表明PECAM-1可能与缺氧诱导的PMN粘附内皮细胞无关。
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Role of PECAM-1 in the adherence of PMN to hypoxic endothelial cells.

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.

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