Reactive oxygen species in vascular endothelial cell motility. Roles of NAD(P)H oxidase and Rac1.

Published

Journal Article (Review)

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.

Full Text

Duke Authors

Cited Authors

  • Moldovan, L; Mythreye, K; Goldschmidt-Clermont, PJ; Satterwhite, LL

Published Date

  • July 2006

Published In

Volume / Issue

  • 71 / 2

Start / End Page

  • 236 - 246

PubMed ID

  • 16782079

Pubmed Central ID

  • 16782079

Electronic International Standard Serial Number (EISSN)

  • 1755-3245

International Standard Serial Number (ISSN)

  • 0008-6363

Digital Object Identifier (DOI)

  • 10.1016/j.cardiores.2006.05.003

Language

  • eng