| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6108640 | Journal of Hepatology | 2009 | 11 Pages |
Abstract
ESAM is expressed in the postischemic liver and mediates neutrophil but not T-cell transmigration during early reperfusion. ESAM deficiency attenuates I/R-induced vascular leakage and does not affect leukocyte adherence. Despite the effect on neutrophil migration, ESAM-deficiency does not protect from I/R-induced injury.
Keywords
FITCPECAM-1hpfI/RROSCell injuryischemia-reperfusionterminal deoxynucleotidyl transferase-mediated dUTP nick end-labelingTUNELApoptosishigh-power fieldsT-cellsEndothelial cellsfluorescein isothiocyanateESAMJAMplatelet endothelial cell adhesion molecule-1junctional adhesion moleculeVascular leakageNeutrophilsReactive oxygen species
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Authors
Andrej Khandoga, Stefanie Huettinger, Alexander G. Khandoga, Hang Li, Stefan Butz, Karl-Walter Jauch, Dietmar Vestweber, Fritz Krombach,