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J. Biol. Chem., Vol. 277, Issue 17, 14390-14399, April 26, 2002
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From the Human immunodeficiency virus infection is
associated with inflammation and endothelial cell activation that
cannot be ascribed to direct infection by the virus or to the presence
of opportunistic infections. Factors related to the virus itself, to
the host and/or to environmental exposures probably account for these
observations. The HIV protein Tat, a viral regulator required for
efficient transcription of the viral genome in host cells is secreted
from infected cells and taken up by uninfected by-stander cells. Tat can also act as a general transcriptional activator of key inflammatory molecules. We have examined whether Tat contributes to this endothelial cell activation by activating NF-
The Human Immunodeficiency Virus-1 Tat Protein Activates
Human Umbilical Vein Endothelial Cell E-selectin Expression via an
NF-
B-dependent Mechanism*
,,,,
, and**
Webb-Waring Institute for Cancer, Aging and
Antioxidant Research, the ¶ Department of Microbiology, and
the Department of Pharmaceutical Sciences, School of Pharmacy,
University of Colorado Health Sciences Center, Denver, Colorado 80262, and the § Department of Molecular and Cellular Physiology,
Louisiana State University Medical Center, Shreveport, Louisiana
71130
B. Human endothelial cells exposed to Tat in the culture medium activated E-selectin expression with delayed kinetics compared with tumor necrosis factor (TNF).
Tat-mediated E-selectin up-regulation required the basic domain of Tat
and was inhibited by a Tat antibody. Transfection of human E-selectin promoter-luciferase reporter constructs into Tat-bearing cells or into
endothelial cells co-transfected with a Tat expression vector resulted
in induction of luciferase expression. Either Tat or TNF activated p65
translocation and binding to an oligonucleotide containing the
E-selectin B site 3 sequence. Tat-mediated p65 translocation was
also delayed compared with TNF. Neither agent induced new synthesis of
p65. A super-repressor adenovirus (AdIB
SR) that constitutively
sequesters IB in the cytoplasm as well as cycloheximide or
actinomycin D inhibited Tat- or TNF-mediated B translocation and
E-selectin up-regulation.
*
This work was supported by National Institutes of Health
NHLBI Grants HL59785 (to S. C. F. and A. C. G.) and
HL58344 (to J. S.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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