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Am J Physiol Endocrinol Metab 275: E479-E486, 1998;
0193-1849/98 $5.00
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Vol. 275, Issue 3, E479-E486, September 1998

Endotoxin-induced migration of monocytes and PECAM-1 phosphorylation are abrogated by PAF receptor antagonists

Yamin Shen1, Chand Sultana1, Moshe Arditi2, Kwang Sik Kim2, and Vijay K. Kalra1

1 Departments of Biochemistry and Molecular Biology and 2 Division of Infectious Diseases, Childrens Hospital Los Angeles, University of Southern California School of Medicine, Los Angeles, California 90033

The trafficking of monocytes across the endothelial lining of the blood vessel increases in response to bacterial infection at sites of inflammation. However, the molecular events involved in the diapedesis of monocytes in response to endotoxin are not completely understood. Our studies revealed that signaling by lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVEC) resulted in a threefold increase in the transendothelial migration of monocyte-like HL-60 cells and a sevenfold increase in the phosphorylation of platelet endothelial cell adhesion molecule-1 (PECAM-1). The transmigration induced by LPS was inhibited by an antibody to PECAM-1. Both the phosphorylation of PECAM-1 and transendothelial migration of monocytes were inhibited by a platelet-activating factor (PAF) receptor antagonist, indicating the autocrine effect of PAF in these events. Treatment of HUVEC with LPS caused a fourfold increase in PAF receptor mRNA expression that was completely blocked by the PAF receptor antagonist. We conclude that PAF, generated by HUVEC in response to LPS or gram-negative bacterial infection, acts in an autocrine manner, causing PECAM-1 phosphorylation and thus the transendothelial migration of monocytes.

endothelial cells; lipopolysaccharide; platelet endothelial cell adhesion molecule-1; platelet-activating factor; transendothelial migration; diapedesis


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