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Received for publication December 10, 2002.
Revised January 2, 2003.
Accepted for publication January 30, 2003.
in
Endothelial Cells
Oxidative signals play an important role in the regulation
of endothelial cell adhesion molecule expression. Small
GTP-binding protein Rac1 is activated by various
proinflammatory substances and regulates superoxide
generation in endothelial cells (EC). In the present
study, we demonstrate that adenoviral-mediated expression
of dominant negative N17Rac1 (Ad.N17Rac1) suppresses
TNF-
induced vascular cell adhesion molecule-1
(VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and
E-selectin gene expression in a dose dependent manner.
Ad.N17Rac1 did not inhibit TNF- induced activation
of nuclear NF-
B binding activity or
IB- degradation. In contrast, Ad.N17Rac1
inhibited TNF- induced NF-B-driven
HIV(B)4CAT and p288VCAM-Luc promoter activity,
suggesting that N17Rac1 inhibits TNF- induced
VCAM-1, E-selectin and ICAM-1 through suppressing
NF-B mediated transactivation. In addition,
expression of superoxide dismutase by adenovirus
suppressed TNF- induced VCAM-1, E-selectin and
ICAM-1 mRNA accumulation. However, adenoviral mediated
expression of catalase only partially inhibited
TNF- induced E-selectin gene expression, and had
no effect on VCAM-1 and ICAM-1 gene expression. These
data suggest that Rac1 and superoxide play crucial roles
in the regulation of expression of cell adhesion molecules
in endothelial cells.
Key words:
E-selectin, endothelial cell, intercellular adhesion molecule-1, rac1, superoxide, vsacular cell adhesion molecule-1
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