Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-1-26
pubmed:abstractText
Although hypoxia stimulates the expression of vascular endothelial growth factor (VEGF), little is known of the role or mechanism by which VEGF functions after ischemia and reperfusion (I/R) injury. In this report, we first evaluated the expression of VEGF in a mouse model of liver warm ischemia. We found that the expression of VEGF increased after ischemia but peaked between 2 and 6 hours after reperfusion. Mice were treated with a neutralizing anti-mouse VEGF antiserum (anti-VEGF) or control serum daily from day -1 (1 day before the initiation of ischemia). Treatment with anti-VEGF significantly reduced serum glutaminic pyruvic transaminase levels and reduced histological evidence of hepatocellular damage compared with controls. Anti-VEGF also markedly decreased T-cell, macrophage, and neutrophil accumulation within livers and reduced the frequency of intrahepatic apoptotic terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling-positive cells. Moreover, there was a reduction in the expression of pro-inflammatory cytokines (tumor necrosis factor-alpha and interferon-gamma), chemokines (interferon-inducible protein-10 and monocyte chemoattractant protein-1) and adhesion molecules (E-selectin) in parallel with enhanced expression of anti-apoptotic genes (Bcl-2/Bcl-xl and heme oxygenase-1) in anti-VEGF-treated animals. In conclusion, hypoxia-inducible VEGF expression by hepatocytes modulates leukocyte trafficking and leukocyte-induced injury in a mouse liver model of warm I/R injury, demonstrating the importance of endogenous VEGF production in the pathophysiology of hepatic I/R injury.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-10450732, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-10617467, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-10699162, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-11090063, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-11283668, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-11435348, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-11571441, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12084990, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12177608, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12215270, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12394829, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12540779, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12710939, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12775431, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-1279431, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-1279432, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12859717, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-12874247, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-14660742, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-14739103, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-15210576, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-15646818, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-15880052, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-15919761, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-16007247, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-7531342, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-7540725, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-7584949, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-7685932, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-7768934, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-8709735, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-9034784, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-9054767, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-9151791, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-9271438, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-9346879, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-9354516, http://linkedlifedata.com/resource/pubmed/commentcorrection/16436682-9665379
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9440
pubmed:author
pubmed:issnType
Print
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
695-705
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:16436682-Humans, pubmed-meshheading:16436682-Animals, pubmed-meshheading:16436682-Mice, pubmed-meshheading:16436682-Liver Diseases, pubmed-meshheading:16436682-Umbilical Veins, pubmed-meshheading:16436682-Rabbits, pubmed-meshheading:16436682-Male, pubmed-meshheading:16436682-Macrophages, pubmed-meshheading:16436682-Cells, Cultured, pubmed-meshheading:16436682-Endothelium, Vascular, pubmed-meshheading:16436682-Neutrophils, pubmed-meshheading:16436682-Immunoglobulin G, pubmed-meshheading:16436682-Mice, Inbred C57BL, pubmed-meshheading:16436682-T-Lymphocytes, pubmed-meshheading:16436682-Chemotaxis, Leukocyte, pubmed-meshheading:16436682-Apoptosis, pubmed-meshheading:16436682-Reperfusion Injury, pubmed-meshheading:16436682-Cytokines, pubmed-meshheading:16436682-Vascular Endothelial Growth Factor A
More...