culosis, hepatitis, and the human immunodeficiency virus/ This study tested the hypothesis that prolonged conacquired immune deficiency syndrome. Paradoxically, sumption of alcohol directly or indirectly, through endochronic alcohol intoxication may activate some aspects of nontoxin influx in the ci
Monocyte chemoattractant protein-1 enhances expression of intercellular adhesion molecule-1 following ischemia-reperfusion of the liver in rats
β Scribed by Yasuo Yamaguchi; Fujio Matsumura; Motohiro Takeya; Osamu Ichiguchi; Jun-Ichi Kuratsu; Tadashi Horiuchi; Eiji Akizuki; Teishi Matsuda; Kazutoshi Okabe; Hajime Ohshiro; Jian Liang; Katsutaka Mori; Shinwa Yamada; Kiyoshi Takahashi; Michio Ogawa
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 172 KB
- Volume
- 27
- Category
- Article
- ISSN
- 0270-9139
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β¦ Synopsis
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-1 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-5 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.
π SIMILAR VOLUMES
We investigated the role of anticoagulant in the ischemia/reperfusion injury of the liver, using activated protein C (APC), active human urinary thrombomodulin (UTM), and factor Xa blocked at the active site (DEGR-Xa). Liver ischemia was induced in male Wistar rats by occlusion of the portal vein wi