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Blood, Vol. 93 No. 11 (June 1), 1999:
pp. 3685-3693
Monocyte Arrest and Transmigration on Inflamed Endothelium in Shear
Flow Is Inhibited by Adenovirus-Mediated Gene Transfer of I B-
Kim S.C. Weber,
Georg Draude,
Wolfgang Erl,
Rainer de Martin, and
Christian Weber
From the Institut für Prophylaxe und Epidemiologie der
Kreislaufkrankheiten, Ludwig-Maximilians Universität,
München, Germany; the Karolinska Hospital, Centre of Molecular
Medicine L8:03, Stockholm, Sweden; and the Vienna International
Research Center, Department of Vascular Biology, Vienna, Austria.
Mobilization of nuclear factor- B (NF-B) activates
transcription of genes encoding endothelial adhesion molecules and
chemokines that contribute to monocyte infiltration critical in
atherogenesis. Inhibition of NF-B has been achieved by
pharmacological and genetic approaches; however, monocyte interactions
with activated endothelium in shear flow following gene transfer of the
NF-B inhibitor IB- have not been studied. We found that
overexpression of IB- in endothelial cells using a recombinant
adenovirus prevented tumor necrosis factor- (TNF-)-induced
degradation of IB- and suppressed the upregulation of vascular
cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1
(ICAM-1), and E-selectin mRNA and surface protein expression and the
upregulation of transcripts for the chemokines monocyte chemoattractant
protein 1 (MCP-1) and growth-related activity- (GRO-) by
TNF-. This was associated with a reduction in
endothelial MCP-1 secretion and GRO- immobilization. Adhesion assays
under physiological shear flow conditions showed that firm arrest,
spreading, and transmigration of monocytes on TNF--activated
endothelium was markedly inhibited by IB- overexpression. Inhibition with monoclonal antibodies and peptide antagonists inferred
that this was due to reduced expression of Ig integrin ligand as well
as of chemokines specifically involved in these events. In contrast,
rolling of monocytes was increased by IB- transfer and was partly
mediated by P-selectin; however, it appeared to be unaffected by the
inhibition of E-selectin induction. Thus, our data provide
novel evidence that selective modulation of NF-B by adenoviral
transfer of IB- impairs the expression of multiple endothelial
gene products required for subsequent monocyte arrest and emigration in
shear flow and thus for monocyte infiltration in atherosclerotic plaques.
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