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Title

NADPH oxidase 1 deficiency alters caveolin phosphorylation and angiotensin II-receptor localization in vascular smooth muscle
Authors
Basset, Olivier
Deffert-Delbouille, Christine
Foti, Michelangelo
Bedard, Karen
Jaquet, Vincent
Ogier-Denis, Eric
Krause, Karl-Heinz
Published in Antioxidants & Redox Signaling. 2009, vol. 11, no. 10, p. 2371-84
Abstract The superoxide-generating NADPH oxidase NOX1 is thought to be involved in signaling by the angiotensin II-receptor AT1R. However, underlying signaling steps are poorly understood. In this study, we investigated the effect of AngII on aortic smooth muscle from wild-type and NOX1-deficient mice. NOX1-deficient cells showed decreased basal ROS generation and did not produce ROS in response to AngII. Unexpectedly, AngII-dependent Ca(2+) signaling was markedly decreased in NOX1-deficient cells. Immunostaining demonstrated that AT1R was localized on the plasma membrane in wild-type, but intracellularly in NOX1-deficient cells. Immunohistochemistry and immunoblotting showed a decreased expression of AT1R in the aorta of NOX1-deficient mice. To investigate the basis of the abnormal AT1R targeting, we studied caveolin expression and phosphorylation. The amounts of total caveolin and of caveolae were not different in NOX1-deficient mice, but a marked decrease occurred in the phosphorylated form of caveolin. Exogenous H(2)O(2) or transfection of a NOX1 plasmid restored AngII responses in NOX1-deficient cells. Based on these findings, we propose that NOX1-derived reactive oxygen species regulate cell-surface expression of AT1R through mechanisms including caveolin phosphorylation. The lack cell-surface AT1R expression in smooth muscle could be involved in the decreased blood pressure in NOX1-deficient mice.
Keywords Angiotensin II/genetics/metabolism — Animals — Aorta/anatomy & histology — Calcium/metabolism — Caveolins/metabolism — Cells, Cultured — Mice — Mice, Inbred C57BL — Mice, Knockout — Muscle, Smooth, Vascular/cytology/metabolism — Myocytes, Smooth Muscle/cytology/metabolism — NADH, NADPH Oxidoreductases/deficiency/genetics — Phosphorylation — Reactive Oxygen Species/metabolism — Receptor, Angiotensin, Type 1/genetics/metabolism — Signal Transduction/physiology
Identifiers
PMID: 19309260
Full text
Article (Published version) (688 Kb) - document accessible for UNIGE members only Limited access to UNIGE
Structures
Faculté de médecine / Section de médecine fondamentale / Département de pathologie et immunologie
Faculté de médecine / Section de médecine fondamentale / Département de physiologie cellulaire et métabolisme
Research groups Groupe Schaller Karl Lothard (neurochirurgie) (851)
Obésité et syndrome métabolique (803)
Radicaux libres et cellules souches embryonnaires (60)
Citation
(ISO format) 		BASSET, Olivier et al. NADPH oxidase 1 deficiency alters caveolin phosphorylation and angiotensin II-receptor localization in vascular smooth muscle. In: Antioxidants & redox signaling, 2009, vol. 11, n° 10, p. 2371-84. doi: 10.1089/ARS.2009.2584 https://archive-ouverte.unige.ch/unige:5405

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Deposited on : 2010-03-12

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