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1 Department of Pharmacology and 2 Department of Immunology and Microbiology, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois 60612
Reactive oxygen
species (ROS) are generated at sites of inflammation and injury, and at
low levels, ROS can function as signaling molecules participating as
signaling intermediates in regulation of fundamental cell activities
such as cell growth and cell adaptation responses, whereas at higher
concentrations, ROS can cause cellular injury and death. The vascular
endothelium, which regulates the passage of macromolecules and
circulating cells from blood to tissues, is a major target of oxidant
stress, playing a critical role in the pathophysiology of several
vascular diseases and disorders. Specifically, oxidant stress increases
vascular endothelial permeability and promotes leukocyte adhesion,
which are coupled with alterations in endothelial signal transduction
and redox-regulated transcription factors such as activator protein-1
and nuclear factor-
B. This review discusses recent findings
on the cellular and molecular mechanisms by which ROS signal events
leading to impairment of endothelial barrier function and promotion of
leukocyte adhesion. Particular emphasis is placed on the regulation of
cell-cell and cell-surface adhesion molecules, the actin cytoskeleton,
key protein kinases, and signal transduction events.
endothelial permeability; leukocyte transmigration; actin filament; cadherin; occludin; intercellular adhesion molecule-1; selectins; redox-sensitive signal transduction; nuclear factor-B
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