PMID- 7919375
OWN - NLM
STAT- MEDLINE
DCOM- 19941109
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 84
IP  - 8
DP  - 1994 Oct 15
TI  - Functional activities of receptors for tumor necrosis factor-alpha on human 
      vascular endothelial cells.
PG  - 2578-90
AB  - Tumor necrosis factor-alpha (TNF-alpha) plays a critical role in the control of 
      endothelial cell function and hence in regulating traffic of circulating cells 
      into tissues in vivo. Stimulation of endothelial cells in vitro by TNF-alpha 
      increases the surface expression of leukocyte adhesion molecules, enhances 
      cytokine production, and induces tissue factor procoagulant activity. In the 
      present study, we have examined the relative roles of the two cell surface 
      receptors for TNF-alpha (p55 and p75) on endothelial cells, using antibodies with 
      both agonistic and antagonistic activities. We report that anti-p55 receptor 
      agonistic antibody Htr-9 induces the expression of tissue factor antigen and the 
      release of interleukin-8 (IL-8) and granulocyte-macrophage colony-stimulating 
      factor (GM-CSF). In contrast, there is very little or no activation of 
      endothelial cell responses by an anti-p75 agonist. TNF-alpha-induced expression 
      of tissue factor and adhesion molecules, and release of IL-8 and GM-CSF, are 
      decreased by antibodies with antagonistic activities for either receptor, 
      although the effect of anti-p55 antibodies is markedly greater than that of 
      anti-p75 antibodies. The responses of endothelial cells to lymphotoxin/TNF-beta 
      are significantly decreased by anti-p55 antagonists alone. Our data suggest that 
      endothelial cell responses to TNF-alpha, such as expression of tissue factor and 
      adhesion molecules for mononuclear cells, which may be important in the 
      pathogenesis of atherosclerosis, are mediated predominantly, but not exclusively, 
      by the p55 TNF receptor.
FAU - Paleolog, E M
AU  - Paleolog EM
AD  - Kennedy Institute of Rheumatology, Sunley Division, London, UK.
FAU - Delasalle, S A
AU  - Delasalle SA
FAU - Buurman, W A
AU  - Buurman WA
FAU - Feldmann, M
AU  - Feldmann M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Antibodies)
RN  - 0 (Antigens, Differentiation, Myelomonocytic)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Cross-Linking Reagents)
RN  - 0 (Interleukin-8)
RN  - 0 (Lymphotoxin-alpha)
RN  - 0 (Platelet Endothelial Cell Adhesion Molecule-1)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - 9035-58-9 (Thromboplastin)
SB  - IM
MH  - Antibodies/pharmacology
MH  - Antigens, Differentiation, Myelomonocytic/metabolism
MH  - Cell Adhesion Molecules/metabolism
MH  - Cell Division/drug effects
MH  - Cross-Linking Reagents
MH  - Endothelium, Vascular/*metabolism
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/metabolism
MH  - Humans
MH  - Interleukin-8/metabolism
MH  - Lymphotoxin-alpha/pharmacology
MH  - Platelet Endothelial Cell Adhesion Molecule-1
MH  - Receptors, Tumor Necrosis Factor/immunology/*physiology
MH  - Thromboplastin/metabolism
MH  - Tumor Necrosis Factor-alpha/*metabolism/pharmacology
MH  - Umbilical Veins
EDAT- 1994/10/15 00:00
MHDA- 1994/10/15 00:01
CRDT- 1994/10/15 00:00
PHST- 1994/10/15 00:00 [pubmed]
PHST- 1994/10/15 00:01 [medline]
PHST- 1994/10/15 00:00 [entrez]
AID - S0006-4971(20)71377-7 [pii]
PST - ppublish
SO  - Blood. 1994 Oct 15;84(8):2578-90.