Monocyte chemoattractant protein-1 enhances expression of intercellular adhesion molecule-1 following ischemia-reperfusion of the liver in rats

被引：58

作者：

Yamaguchi, Y

Matsumura, F

Takeya, M

Ichiguchi, O

Kuratsu, JI

Horiuchi, T

Akizuki, E

Matsuda, T

Okabe, K

Ohshiro, H

Liang, J

Mori, K

Yamada, S

Takahashi, K

Ogawa, M

机构：

[1] Kumamoto Univ, Sch Med, Dept Surg 2, Kumamoto 860, Japan

[2] Kumamoto Univ, Sch Med, Dept Pathol 2, Kumamoto 860, Japan

[3] Kumamoto Univ, Sch Med, Dept Neurosurg, Kumamoto 860, Japan

[4] Daiichi Pharmaceut Co Ltd, Dept Mol Biol, Res Lab, Tokyo, Japan

[5] Univ Occupat & Environm Hlth, Dept Internal Med 1, Kitakyushu, Fukuoka 807, Japan

来源：

HEPATOLOGY | 1998年 / 27卷 / 03期

关键词：

D O I：

10.1002/hep.510270314

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Intercellular adhesion molecule-1 (ICAM-1) is important in neutrophil-dependent injury. We investigated the effects of monocyte chemoattractant protein-1 (MCP-1) produced by Kupffer cells on ICAM-1 expression after ischemia-reperfusion in rat liver by occluding the portal vein for 30 minutes, Serum concentrations of MCP-I increased persistently, By Northern analysis, MCP-1 mRNA increased early and persisted. Kupffer cells harvested 6 hours after reperfusion also expressed this transcript. The transcript and protein also were produced by Kupffer cells from naive controls in response to reactive oxygen species. ICAM-1 mRNA transcripts increased, peaked 3 hours after reperfusion, and decreased gradually thereafter. The level of ICAM-1 mRNA transcripts in the WK-S rat endothelial cell line were markedly enhanced by MCP-1. These results suggest that MCP-1 released by Kupffer cells early after ischemia-reperfusion modulates neutrophil-dependent tissue injury via ICAM-1.

引用

页码：727 / 734

页数：8

共 57 条

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