Substance P induces the expression of intercellular adhesion molecule-1 on vascular endothelial cells and enhances neutrophil transendothelial migration.
To determine whether substance P induces the expression of adhesion molecules ICAM-1 and VCAM-1 on vascular endothelial cells, we examined the effect of substance P, its carboxyl- and amino-terminal peptides, and neurokinin A on the expression of ICAM-1 and VCAM-1 on cultured human umbilical vein endothelial cells (HUVEC). Substance P and the carboxyl-terminal peptide SP(6-11), but not the amino-terminal peptide SP(1-9) or neurokinin A, increased ICAM-1 expression on HUVEC. In contrast, substance P did not significantly induce VCAM-1 expression on HUVEC. Furthermore, stimulation of HUVEC with substance P increased neutrophil transendothelial migration through an ICAM-1-dependent mechanism, as indicated by the inhibitory effect of anti-ICAM-1 antibody. These results indicate that substance P induces ICAM-1 expression on vascular endothelial cells and thereby enhances neutrophil transendothelial migration.
D000911:Antibodies, Monoclonal; D002465:Cell Movement; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis* / Q000276:immunology; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects*; D013268:Stimulation, Chemical; D013373:Substance P / Q000494:pharmacology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis*
D000911:Antibodies, Monoclonal; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D013373:Substance P