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Author Notes:

Address correspondence to: Dr. W. Robert Taylor, Division of Cardiology, Emory University School of Medicine, 1639 Pierce Drive, Suite 319 WMB, Atlanta, GA, 30322. E-mail:wtaylor@emory.edu


Research Funding:

This work was supported by NIH RO1 HL70531, NIH RO1 HL090584, NIH RO1 HL096796-01 (NM), NIH UO1HL080711, and a predoctoral research fellowship from the Southeast Affiliate of the American Heart Association.

Redox Signaling in an In Vivo Murine Model of Low Magnitude Oscillatory Wall Shear Stress


Journal Title:

Antioxidants and Redox Signaling


Volume 15, Number 5


, Pages 1369-1378

Type of Work:

Article | Post-print: After Peer Review


Abstract Wall Shear Stress (WSS) has been identified as an important factor in the pathogenesis of atherosclerosis. We utilized a novel murine aortic coarctation model to acutely create a region of low magnitude oscillatory WSS in vivo. We employed this model to test the hypothesis that acute changes in WSS in vivo induce upregulation of inflammatory proteins, mediated by reactive oxygen species (ROS). Superoxide generation and VCAM-1 expression both increased in regions of low magnitude oscillatory WSS. WSS-dependent superoxide formation was attenuated by tempol treatment, but was unchanged in p47 phox knockout (ko) mice. However, in both the p47 phox ko mice and the tempol-treated mice, low magnitude oscillatory WSS produced an increase in VCAM-1 expression comparable to control mice. Additionally, this same VCAM-1 expression was observed in ebselen-treated mice and catalase overexpressing mice. These results suggest that although the redox state is important to the overall pathogenesis of atherosclerosis, the initial WSS-dependent inflammatory response leading to lesion localization is not dependent on ROS. Antioxid. Redox Signal. 15, 1369–1378.

Copyright information:

© 2011, Mary Ann Liebert, Inc.

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