Human recombinant interleukin-1 beta- and tumor necrosis factor alpha-mediated suppression of heparin-like compounds on cultured porcine aortic endothelial cells

Journal Article · Sat Sep 01 04:00:00 EDT 1990 · Journal of Cellular Physiology; (USA)

OSTI ID:6511681

Kobayashi, M; Shimada, K; Ozawa, T ^[1]

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1. Kochi Medical School (Japan)

Cytokines are known to tip the balance of the coagulant-anticoagulant molecules on the endothelial cell surface toward intravascular coagulation. Their effects on endothelial cell surface-associated heparin-like compounds have not been examined yet. Incorporation of (35S)sulfate into heparan sulfate on cultured porcine aortic endothelial cells was suppressed by human recombinant interleukin-1 beta (rIL-1 beta) or tumor necrosis factor alpha (rTNF alpha) in a dose- and time-dependent manner with little effect on cell number, protein content, and (3H)leucine incorporation of cells. Maximal inhibition was achieved by incubation of cells with 100 ng/ml of rIL-1 beta or 5 ng/ml of rTNF alpha for 12-24 hours, resulting in a reduction of the synthesis of heparan sulfate on the cell surface by approximately 50%. The dose dependency was consistent with that seen in the stimulation of endothelial cell procoagulant activity by each cytokine. The suppression of heparan sulfate synthesis was sustained for at least 48 hours after pretreatment of cells with cytokines and was unchanged after the addition of indomethacin or polymyxin B. The rate of degradation of prelabeled 35S-heparan sulfate on the cell surface was not altered by cytokine treatments. Neither the size, the net negative charge, nor the proportion of the molecule with high affinity for antithrombin III of endothelial cell heparan sulfate was changed by cytokines. Furthermore, specific binding of 125I-labeled antithrombin III to the endothelial cell surface was reduced to 40-60% of control by cytokines. In parallel with reduction in binding, antithrombin III cofactor activity was partially diminished in cytokine-treated endothelial cells. Thus, cytokine-mediated suppression of heparin-like substance on endothelial cells appears to be another cytokine-inducible endothelial effects affecting coagulation.

• OSTI ID: 6511681
• Journal Information: Journal of Cellular Physiology; (USA), Journal Name: Journal of Cellular Physiology; (USA) Vol. 144:3; ISSN 0021-9541; ISSN JCLLA
• Country of Publication: United States
• Language: English

Related Subjects

550201* -- Biochemistry-- Tracer Techniques
59 BASIC BIOLOGICAL SCIENCES
AMINES
AMINO ACIDS
ANIMAL TISSUES
ANIMALS
ANTICOAGULANTS
AORTA
ARTERIES
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BIOCHEMICAL REACTION KINETICS
BLOOD VESSELS
BODY
CARBOHYDRATES
CARBOXYLIC ACIDS
CARDIOVASCULAR SYSTEM
CELL CONSTITUENTS
CELL MEMBRANES
DAYS LIVING RADIOISOTOPES
DOMESTIC ANIMALS
DOSE-RESPONSE RELATIONSHIPS
DRUGS
ELECTRON CAPTURE RADIOISOTOPES
ENDOTHELIUM
EVEN-ODD NUCLEI
GROWTH FACTORS
HEMATOLOGIC AGENTS
HEPARIN
HYDROGEN COMPOUNDS
INTERMEDIATE MASS NUCLEI
IODINE 125
IODINE ISOTOPES
ISOTOPE APPLICATIONS
ISOTOPES
KINETICS
LEUCINE
LIGHT NUCLEI
LYMPHOKINES
MAMMALS
MAN
MEMBRANES
MITOGENS
MUCOPOLYSACCHARIDES
NUCLEI
ODD-EVEN NUCLEI
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANIC SULFUR COMPOUNDS
ORGANS
OXYGEN COMPOUNDS
POLYSACCHARIDES
PRIMATES
PROTEINS
RADIOISOTOPES
REACTION KINETICS
SACCHARIDES
SULFATES
SULFUR 35
SULFUR COMPOUNDS
SULFUR ISOTOPES
SWINE
TIME DEPENDENCE
TISSUES
TRACER TECHNIQUES
TRITIUM COMPOUNDS
VERTEBRATES