Neutrophil killing of human umbilical vein endothelial cells is oxygen radical-mediated and enhanced by TNF-. alpha

Conference · Mon Mar 11 04:00:00 EST 1991 · FASEB Journal (Federation of American Societies for Experimental Biology); (United States)

OSTI ID:5751684

Dame, M K; Varani, J; Weinberg, J M; Ward, P A ^[1]

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1. Univ. of Michigan, Ann Arbor (United States)

Human umbilical vein endothelial cells are sensitive to killing by activated human neutrophils. Killing is inhibited in the presence of catalase and deferoxamine mesylate but not soybean trypsin inhibitor. Reagent hydrogen peroxide can substitute for activated neutrophils in producing endothelial cell injury. These data suggest that lethal injury is due to the production of oxygen radicals by activated neutrophils. In these respects, the human umbilical vein endothelial cells are similar to rat pulmonary artery endothelial cells in that pretreatment with TNF-{alpha} increases sensitivity to injury by activated neutrophils. In part, the increased endothelial cell sensitivity to killing by neutrophils may be due to up-regulation of surface adhesion molecules. However, it was observed that cells passaged more than two times in culture did not demonstrate increased killing after treatment with TNF-{alpha} while up-regulation of neutrophil adhesion could be detected through several additional passages. Although the human umbilical vein endothelial cells are qualitatively similar to rat pulmonary artery endothelial cells in their sensitivity to killing, they are quantitatively much more resistant. What accounts for the relative resistance of the human umbilical vein endothelial cells is not fully understood. In the rat pulmonary artery endothelial cells, killing is known to be dependent on an intraendothelial source of iron. Pre-treatment of the human umbilical vein endothelial cells with 8-hydroxyquinoline-bound iron increased their sensitivity to oxidant injury. These data suggest that the availability of iron within the human umbilical vein endothelial cells may be a limiting factor in sensitivity to oxygen radical-mediated injury.

• OSTI ID: 5751684
• Report Number(s): CONF-9104107--
• Conference Information: Journal Name: FASEB Journal (Federation of American Societies for Experimental Biology); (United States) Journal Volume: 5:4
• Country of Publication: United States
• Language: English

Related Subjects

560300* -- Chemicals Metabolism & Toxicology
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ANIMAL CELLS
ANIMAL TISSUES
ANIMALS
ARTERIES
BIOLOGICAL EFFECTS
BIOLOGICAL MATERIALS
BLOOD
BLOOD CELLS
BLOOD VESSELS
BODY
BODY FLUIDS
CARDIOVASCULAR SYSTEM
CELL KILLING
COMPARATIVE EVALUATIONS
ELEMENTS
ENDOTHELIUM
ENZYME INHIBITORS
EVALUATION
GROWTH FACTORS
HYDROGEN COMPOUNDS
HYDROGEN PEROXIDE
IRON
LEUKOCYTES
LUNGS
LYMPHOKINES
MAMMALS
MAN
MATERIALS
METALS
MITOGENS
NEUTROPHILS
ORGANIC COMPOUNDS
ORGANS
OXYGEN COMPOUNDS
PEROXIDES
PRIMATES
PROTEINS
RADICALS
RATS
RESPIRATORY SYSTEM
RODENTS
SENSITIVITY
TISSUES
TOXICITY
TRANSITION ELEMENTS
VEINS
VERTEBRATES