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1 Medicine, Division of Cardiology, Emory University, Atlanta, Georgia, United States
2 Medicine, Division of Cardiology, Emory University, Atlanta, Georgia, United States; , United States
* To whom correspondence should be addressed. E-mail: kgriend{at}emory.edu.
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. Compared with control m+/+ mice, aortas from 4- and 12-week-old db/db mice had higher NADPH oxidase activity and increased superoxide levels, leading to NADPH oxidase-dependent impaired vasodilation at 12 weeks. Diabetes progression from 4-12 weeks 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 (BMP4) and osteopontin (OPN). After 8 weeks of treatment with the superoxide scavenger tempol, 12-week db/db mice had lower superoxide production, reduced plasma glucose and lipids, and lower BMP4 and OPN protein expression compared with non-treated 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 BMP4, but not CTGF, induction suggests that DM-induced vascular inflammation involves both ROS-sensitive and -insensitive pathways.
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