Copyright © 2006, European Society of Cardiology
Reactive oxygen species in vascular endothelial cell motility. Roles of NAD(P)H oxidase and Rac1
aDavis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, United States
bDepartment of Medicine, Duke University Medical Center, Bell Research Building, Room 345, Durham, NC 27710, United States
cLeonard M. Miller School of Medicine at the University of Miami, P. O. Box 016099, Miami, FL 33101, United States
* Corresponding author. Tel.: +1 919 681 0381. Email address: lisa.satterwhite{at}duke.edu
Reactive oxygen species (ROS) are acknowledged generally to be multi-faceted regulators of cellular functions that trigger various pathological states when present chronically or transiently at non-physiologically high levels. Here we focus on the physiological involvement of ROS in cellular motility, with special emphasis on endothelial cells (EC). An important source of ROS within EC is the non-phagocytic NAD(P)H oxidase, and the small GTPase Rac1 plays a central role in activating this complex. Rac1 is one of the three Rho-family molecules (Rac, Rho and Cdc42) involved in the control of the actin cytoskeleton in response to various signals. In this review we examine the evidence linking ROS production, Rac1 activation and actin organization to EC motility, considering mechanisms for direct interaction of ROS and actin and the effects of ROS on proteins that regulate the actin cytoskeleton. The accumulated evidence suggests that ROS are important regulators of the actin cytoskeletal dynamics and cellular motility, and more in-depth studies are needed to understand the underlying mechanisms.
KEYWORDS Redox signalling; Endothelial function; NADPH oxidase; Oxygen radicals; Cytoskeleton
Time for primary review 23 days
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