Altered Expression of Endothelin, Vascular Endothelial Growth Factor, and Its Receptor in Hepatic Tissue in Endotoxemic Rat.
From: Department of Cardiovascular Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
Experimental biology and medicine (Maywood, N.J.)
- Publish Date: Jun 2006
- ISSN: 1535-3702
- Volume: 231
- Issue: 6
- Pages: 1182-6
- Medium: Print
- Language: English
- Citation (JAMA): Zaedi Sohel, Jesmin Subrina, Yamaguchi Naoto, et al. Altered Expression of Endothelin, Vascular Endothelial Growth Factor, and Its Receptor in Hepatic Tissue in Endotoxemic Rat.. Exp. Biol. Med. (Maywood) Jun 2006;231:1182-6
Abstract
Sepsis involves a heterogeneous class of syndromes, and septic shock, a severe form of sepsis, is associated with the development of progressive damage in multiple organs. The present study examined the time-dependent alterations of endothelin-1 (ET-1) and vascular endothelial growth factor (VEGF) levels in liver tissue in a septic rat model. Healthy male Wistar rats aged 15 weeks received 15 mg/kg lipopolysaccharide (LPS) and were sacrificed at different time points (1, 3, 6, and 10 hrs after treatment). Rats that did not receive LPS were considered to be controls. A 28-fold increase in the ET-1 level was observed in liver tissue 10 hrs after LPS administration. VEGF was also altered in hepatic tissue in a time-dependent manner. A gradual increase of VEGF expression in liver tissue after LPS administration was observed. Expression of Flt-1, the vascular permeability receptor of VEGF, was also increased in liver tissue after LPS administration. ET-1 is a potent vasoconstrictor and, therefore, may play a role in the regulation of hepatic perfusion in a sepsis model. On the other hand, VEGF may be involved in capillary leakage in liver tissue after LPS administration. The present findings suggest that there might be a loss of balance between the ET-1 and VEGF levels in the septic liver at different time points, which could contribute to the pathogenesis of acute liver injury in endotoxemia.
Mesh Headings (Keywords): Animals, Blood Pressure, Disease Models, Animal, Endothelin-1, Lipopolysaccharides, Liver, Male, Necrosis, Neutrophil Infiltration, Rats, Rats, Wistar, Time Factors, Vascular Endothelial Growth Factor A
Check for Full Text / PubMed Unique Identifier (PMID): 16741073
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