Nakagawa N, Sano H, Iwamoto I
Department of Internal Medicine, Chiba University School of Medicine, Japan.
Peptides. 1995;16(4):721-5. doi: 10.1016/0196-9781(95)00037-k.
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.
为了确定P物质是否能诱导血管内皮细胞上细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）的表达，我们检测了P物质、其羧基末端和氨基末端肽以及神经激肽A对培养的人脐静脉内皮细胞（HUVEC）上ICAM-1和VCAM-1表达的影响。P物质和羧基末端肽SP(6 - 11)可增加HUVEC上ICAM-1的表达，但氨基末端肽SP(1 - 9)或神经激肽A则不能。相反，P物质并未显著诱导HUVEC上VCAM-1的表达。此外，如抗ICAM-1抗体的抑制作用所示，用P物质刺激HUVEC可通过依赖ICAM-1的机制增加中性粒细胞跨内皮迁移。这些结果表明，P物质可诱导血管内皮细胞上ICAM-1的表达，从而增强中性粒细胞跨内皮迁移。
