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Am J Physiol Heart Circ Physiol 292: H2073-H2082, 2007. First published January 19, 2007; doi:10.1152/ajpheart.00943.2006
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Cardiovascular-Renal Mechanisms in Health and Disease

Reactive oxygen species-selective regulation of aortic inflammatory gene expression in Type 2 diabetes

Alejandra San Martín,* Pingfeng Du,* Anna Dikalova, Bernard Lassègue, María Aleman, María Carolina Góngora, Kathryn Brown, Giji Joseph, David G. Harrison, W. Robert Taylor, Hanjoong Jo, and Kathy K. Griendling

Division of Cardiology, Department of Medicine, Emory University, Atlanta, Georgia

Submitted 31 August 2006 ; accepted in final form 16 January 2007

Vascular diseases are a major complication of diabetes mellitus (DM), although their etiology is poorly understood. NADPH oxidase-derived reactive oxygen species (ROS) production and inflammation are potential mediators of DM-associated vascular diseases. Using db/db mice as a Type 2 diabetes model, we examined the relationship between NADPH oxidase-derived ROS and vascular inflammation. When compared with control m+/+ mice, aortas from 4- and 12-wk-old db/db mice had higher NADPH oxidase activity and increased superoxide levels, leading to NADPH oxidase-dependent impaired vasodilation at 12 wk. Diabetes progression from 4 to 12 wk led to increased Nox1, Nox4, and p22phox subunit mRNAs and induced the expression of a group of matrix remodeling-related cytokines: connective tissue growth factor (CTGF), bone morphogenetic protein 4 (BMP-4), and osteopontin (OPN). After 8 wk of treatment with the superoxide scavenger Tempol, 12-wk-old db/db mice had lower superoxide production, reduced plasma glucose and lipids, and lower BMP-4 and OPN protein expression when compared with nontreated mice. No changes were observed with Tempol in CTGF or m+/+ mice. The ability of Tempol to reverse ROS production as well as OPN and BMP-4, but not CTGF, induction suggests that DM-induced vascular inflammation involves both ROS-sensitive and -insensitive pathways.

vascular inflammation; NADPH oxidases; cytokines; superoxide; metabolic syndrome



Address for reprint requests and other correspondence: K. K. Griendling, Div. of Cardiology, Emory Univ., 319 WMB, 1639 Pierce Dr., Atlanta, GA 30322 (e-mail: kgriend{at}emory.edu)




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