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Blood, Vol. 94 No. 5 (September 1), 1999:
pp. 1673-1682
Induction of Decay-Accelerating Factor by Cytokines or the
Membrane-Attack Complex Protects Vascular Endothelial Cells Against
Complement Deposition
Justin C. Mason,
Helen Yarwood,
Katharine Sugars,
B. Paul Morgan,
Kevin A. Davies, and
Dorian O. Haskard
From the British Heart Foundation (BHF) Cardiovascular Medicine Unit,
National Heart and Lung Institute, and the Rheumatology Unit, Division
of Medicine, Imperial College School of Technology and Medicine,
Hammersmith Hospital, London; and the Department of Medical
Biochemistry, University of Wales College of Medicine, Cardiff, UK.
Vascular endothelium is continuously exposed to complement-mediated
challenge, and this is enhanced during inflammation. Although the
complement-regulatory proteins decay-accelerating factor (DAF), CD59,
and membrane cofactor protein (MCP) protect endothelial cells (ECs)
against complement-mediated injury, the control of their expression and
relative contributions to vascular protection is unclear. We explored
the hypothesis that mechanisms exist which induce upregulation of
complement-regulatory proteins on ECs to maintain vascular function in
inflammation. Tumor necrosis factor alpha (TNF ) and interferon gamma
(IFN ) each increased DAF expression but not CD59 or MCP expression,
and a combination of these cytokines was more potent than either alone.
Cytokine-induced expression depended on increased DAF mRNA and de novo
protein synthesis and was maximal by 72 hours. In addition, assembly of
the membrane-attack complex (MAC) on ECs induced a 3-fold increase in
DAF expression, and this was enhanced by cytokines. DAF upregulation
was not inhibited by protein kinase C (PKC) antagonists. The increase
in DAF was functionally relevant since it reduced complement 3 (C3)
deposition by 40%, and this was inhibited by an anti-DAF monoclonal
antibody. These observations indicate that upregulation of DAF
expression by cytokines or MAC may represent an important feedback
mechanism to maintain the integrity of the microvasculature during
subacute and chronic inflammatory processes involving complement activation.
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