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(Hypertension. 2006;47:16.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Lipid Rafts Take Center Stage in Endothelial Cell Redox Signaling by Death Receptors

From the Canada Research Chair in Hypertension, Kidney Research Centre, Ottawa Health Research Institute, University of Ottawa, Ontario, Canada.

Correspondence to Rhian M Touyz MD, PhD, Canada Research Chair in Hypertension, Ottawa Health Research Institute, University of Ottawa, 451 Smyth Rd, Ottawa, ON, KIH 8M5. E-mail: rtouyz@uottawa.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Reactive oxygen species are important signaling molecules mediating diverse biological effects in vascular cells ranging from cell growth to cell death.¹ The primary enzymatic source of vascular reactive species is the multisubunit NAD(P)H oxidase, expressed and functionally active in endothelial, vascular smooth muscle, and adventitial cells.² Activation of G protein-coupled receptors by vasoactive agents, such as angiotensin II (Ang II), and receptor tyrosine kinases by growth factors, such as epidermal growth factor (EGF), stimulate NAD(P)H oxidase–derived generation of superoxide and hydrogen peroxide in vascular smooth muscle cells, which activate mitogen-activated protein kinase growth signaling pathways and promote cell cycle progression. In pathological conditions associated with vascular injury and remodeling, increased oxidative stress is now considered a fundamental factor underlying proliferation and hypertrophy of vascular smooth muscle cells.^1,2 Paradoxically in endothelial cells, death receptor ligands and proapoptotic agonists, including tumor necrosis factor (TNF) , Fas ligand (FasL), and endostatin, also stimulate NAD(P)H oxidase–mediated production of reactive oxygen species.^3–5 These processes trigger endothelial cell apoptosis, anoikis, and impaired dilation. How then can agonists that promote cell growth and cell death trigger the same redox-sensitive pathways to elicit divergent cellular responses, and what are the mechanisms that link growth/death receptors to NAD(P)H oxidase in vascular cells?

Emerging evidence indicates that lipid microenvironments on the cell surface, known as lipid rafts, may be critically involved in distal redox-sensitive signaling events and ultimate cell fate.^6,7 In vascular smooth muscle cells, Ang II–induced cell growth involves epidermal growth factor receptor (EGFR) transactivation, mediated through redox-sensitive c-Src, . . . [Full Text of this Article]

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