Caveolin-1 is essential for activation of Rac1 and NAD(P)H oxidase after angiotensin II type 1 receptor stimulation in vascular smooth muscle cells: role in redox signaling and vascular hypertrophy.

TitleCaveolin-1 is essential for activation of Rac1 and NAD(P)H oxidase after angiotensin II type 1 receptor stimulation in vascular smooth muscle cells: role in redox signaling and vascular hypertrophy.
Publication TypeJournal Article
Year of Publication2005
AuthorsZuo, L, Ushio-Fukai M, Ikeda S, Hilenski L, Patrushev N, Alexander WR
JournalArteriosclerosis, thrombosis, and vascular biology
Volume25
Issue9
Pagination1824-30
Date Published2005 Sep
ISSN1524-4636
KeywordsActin Cytoskeleton, Angiotensin II, Animals, Caveolin 1, Cells, Cultured, Hypertrophy, Membrane Microdomains, Muscle, Smooth, Vascular, NADPH Oxidase, Oxidation-Reduction, Phosphorylation, Proto-Oncogene Proteins c-akt, rac1 GTP-Binding Protein, Reactive Oxygen Species, Receptor, Angiotensin, Type 1, Receptor, Epidermal Growth Factor, RNA, Small Interfering, Signal Transduction, SOS1 Protein, Tyrosine, Vasoconstrictor Agents
Abstract

Angiotensin II (Ang II) is a potent mediator of vascular hypertrophy in vascular smooth muscle cells (VSMCs). These effects are mediated through the Ang II type 1 receptor (AT1R) and require its trafficking through caveolin-1 (Cav1)-enriched lipid rafts and reactive oxygen species (ROS) derived from Rac1-dependent NAD(P)H oxidase. The specific role(s) of Cav1 in AT1R signaling is incompletely understood.

Alternate JournalArterioscler. Thromb. Vasc. Biol.