This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Weintraub, N. L. Search for Related Content PubMed PubMed Citation Articles by Weintraub, N. L. Pubmed/NCBI databases Compound via MeSH Substance via MeSH

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:4.)
© 2002 American Heart Association, Inc.

Editorials

Nox Response to Injury

Neal L. Weintraub

From the Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City.

Correspondence to Neal L. Weintraub, MD, CV Division, Department of Internal Medicine, University of Iowa College of Medicine, 200 Hawkins Dr, E329 GH, Iowa City, IA 52242. E-mail neal-weintraub@uiowa.edu

Szöcs and colleagues,¹ in this issue of Arteriosclerosis, Thrombosis and Vascular Biology, have added to our understanding of the role of NAD(P)H oxidase and reactive oxygen species in vascular injury. The study was undertaken by using the rat carotid artery balloon injury model, a well-characterized model of neointimal formation. In this model, vascular balloon injury leads to medial smooth muscle cell proliferation and migration across the internal elastic lamina to form the neointima.^2,3 Adventitial myofibroblasts may also migrate across the media and into the neointima within the first week after balloon injury.⁴ The processes of proliferation and migration of smooth muscle cells and fibroblasts in vitro are critically dependent on the production of reactive oxygen species.^5–8 Moreover, several reports suggest that vascular production of reactive oxygen species increases rapidly after balloon injury, and that treatment with nonspecific antioxidant regimens can inhibit experimental neointimal formation.^9–14 Although the relevance of the rat balloon injury model to human post-angioplasty restenosis is questionable,¹⁵ the well-defined kinetics of neointimal formation in this model provide a unique opportunity to explore the cellular and enzymatic sources of reactive oxygen species during vascular cell proliferation and migration in response to injury in vivo.

See page 21

NAD(P)H Oxidases in the Vasculature: Structural and Functional Considerations

Recent studies indicate that nonphagocytic NAD(P)H oxidases are major sources of reactive oxygen species in the vascular wall. Like the phagocytic respiratory burst NADPH oxidase, non-phagocytic NAD(P)H oxidases reduce molecular oxygen to generate superoxide, which is in turn converted to hydrogen peroxide. However, unlike the phagocytic NADPH oxidase, the NAD(P)H oxidases . . . [Full Text of this Article]

This article has been cited by other articles:

				A. Masamune, T. Watanabe, K. Kikuta, K. Satoh, and T. Shimosegawa NADPH oxidase plays a crucial role in the activation of pancreatic stellate cells Am J Physiol Gastrointest Liver Physiol, January 1, 2008; 294(1): G99 - G108. [Abstract] [Full Text] [PDF]

				M. J. Haurani and P. J. Pagano Adventitial fibroblast reactive oxygen species as autacrine and paracrine mediators of remodeling: Bellwether for vascular disease? Cardiovasc Res, September 1, 2007; 75(4): 679 - 689. [Abstract] [Full Text] [PDF]

				A.-C. Ceacareanu, B. Ceacareanu, D. Zhuang, Y. Chang, R. M. Ray, L. Desai, K. E. Chapman, C. M. Waters, and A. Hassid Nitric oxide attenuates IGF-I-induced aortic smooth muscle cell motility by decreasing Rac1 activity: essential role of PTP-PEST and p130cas Am J Physiol Cell Physiol, April 1, 2006; 290(4): C1263 - C1270. [Abstract] [Full Text] [PDF]

				K. Robert, J.-F. Chasse, D. Santiard-Baron, C. Vayssettes, A. Chabli, J. Aupetit, N. Maeda, P. Kamoun, J. London, and N. Janel Altered Gene Expression in Liver from a Murine Model of Hyperhomocysteinemia J. Biol. Chem., August 22, 2003; 278(34): 31504 - 31511. [Abstract] [Full Text] [PDF]