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Nox1 mediates basic fibroblast growth factor-induced migration of vascular smooth muscle cells

Schroder, Katrin
Helmcke, Ina
Palfi, Katalin
Busse, Rudi
Brandes, R. P.
Published in Arteriosclerosis, Thrombosis, and Vascular Biology. 2007, vol. 27, no. 8, p. 1736-1743
Abstract OBJECTIVE: Basic fibroblast growth factor (bFGF) stimulates vascular smooth muscle cell (SMC) migration. We determined whether bFGF increases SMC reactive oxygen-species (ROS) and studied the role of ROS for SMC migration. METHODS AND RESULTS: bFGF rapidly increased rat SMC ROS formation and migration through pathways sensitive to inhibition of NADPH oxidases, PI3-kinase, protein kinase C, and Rac-1. SiRNA directed against the NADPH oxidase Nox4 impaired basal but not bFGF-induced ROS formation and did not affect migration. In contrast, siRNA against Nox1 blocked the agonist-induced ROS generation as well as the bFGF-induced migration. Agonist-induced migration was also attenuated in SMC derived from Nox1 y/- mice and transduction of Nox1 restored normal migration. Likewise, SMC outgrowth in response to bFGF was attenuated in aortic segments from Nox1 y/- mice as compared with Nox1 y/+ mice. bFGF activated JNK but not Src in a Nox1-dependent manner. Consequently, phosphorylation of the adaptor protein paxillin, which is central for migration and secretion of matrix-metalloproteinases, were dependent on Nox1 as well as JNK but not Src. CONCLUSIONS: These data demonstrate that bFGF activates the Nox1-containing NADPH oxidase and that bFGF through a pathway involving ROS and JNK stimulates SMC migration.
Keywords AnimalsAorta/cytologyCell Movement/ physiologyCells, CulturedFibroblast Growth Factor 2/ metabolismMiceMice, Inbred StrainsModels, AnimalMuscle, Smooth, Vascular/ cytology/ metabolismNADPH Oxidase/analysis/ metabolismProbabilityRandom AllocationRatsRats, Inbred StrainsReactive Oxygen Species/metabolismSensitivity and SpecificityTransfection
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PMID: 17541028
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