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(Received for publication, November 28, 1995, and in revised form, April 9, 1996)
From the Department of Pathology and the Molecular Cardiobiology
Program, Boyer Center for Molecular Medicine and the
§ Section of Immunobiology and the Department of Molecular
Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale
University School of Medicine, New Haven, Connecticut 06511
The responses of vascular endothelial cells (EC)
to tumor necrosis factor-
Volume 271, Number 27,
Issue of July 5, 1996
pp. 16317-16322
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
B-
May Contribute to Persistent
NF-B Activation in Human Endothelial Cells
(TNF), interleukin-1 (IL-1), and
phorbol myristate acetate (PMA) were compared with respect to the
kinetics of (i) NF-
B activation, (ii) IB- and IB-
degradation, and (iii) NF-B-dependent cell surface
molecule expression. TNF rapidly (
20 min) and persistently (>20 h)
activates NF-B; IL-1 rapidly activates NF-B, but activity
declines by 3 h and further by 20 h; PMA slowly and
transiently activates NF-B. Untreated EC contain the inhibitory
proteins IB- and IB-. The onset of NF-B activation
correlates with degradation of IB-, but IB- reappears by
4 h without resequestration of NF-B. TNF causes a rapid but
partial (50%) reduction in IB-, which does not recover by
22 h; IL-1 and PMA cause slower and less sustained reductions in
IB-. All three agonists induce de novo expression of
E-selectin (CD62E) and vascular cell adhesion molecule-1 (CD106) and
increase expression of intercellular adhesion molecule-1 (CD54) at
4 h. TNF induces sustained increases in vascular cell adhesion
molecule-1 and intercellular adhesion molecule-1 and increases human
leukocyte antigen class I molecules at 24 h. We conclude that TNF
causes persistent activation of NF-B in human EC and that this may
result from sustained reductions in IB- levels.
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