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 Pagano, P. J. Search for Related Content PubMed PubMed Citation Articles by Pagano, P. J. Related Collections Remodeling Restenosis Restenosis Smooth muscle proliferation and differentiation

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:175.)
© 2001 American Heart Association, Inc.

Editorial

NAD(P)H Oxidase: Marker of the Dedifferentiated Neointimal Smooth Muscle Cell?

P. J. Pagano

From the Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Mich.

Correspondence to P.J. Pagano, PhD, Senior Staff Investigator, Hypertension and Vascular Research Division, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202-2689. E-mail ppagano1@hfhs.org

In recent years, there has been intense interest in vascular NAD(P)H oxidases and their role in vascular injury and atherosclerosis. Balloon injury has been shown to cause large increases in O₂^– stemming from NAD(P)H oxidases,¹ while other studies have shown that hypercholesterolemia and atherosclerosis can induce vascular expression of NADPH oxidase.^{2 3 4} This induction has been implicated in cell phenotype change and proliferation, and a similar process can be inferred to occur during vascular grafting.⁵ Two key studies have demonstrated that overexpression of NAD(P)H oxidase in cells leads to transformation to a proliferative phenotype,^{6 7} and various redox mechanisms transducing this transformation in injury have been elucidated.⁸ On the contrary, other reports have shown that deletion of 2 essential components of phagocyte NAD(P)H oxidase fail to inhibit lesion formation in apoE^–/– mice.^{9 10} However, it remains to be determined whether those components and NAD(P)H oxidase do play a role under conditions in which the renin-angiotensin system is activated.^{11 12}

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, West et al¹³ present exciting findings suggesting a role for NAD(P)H oxidase–expressing cells in intimal hyperplasia after venous bypass. The authors performed elegant immunohistochemical analyses in an attempt to carefully determine the source and state of differentiation of cells in the subintimal space. They found that cells that strongly express p22^phox (an essential NADPH oxidase component) do not express smoothelin, a marker for highly differentiated smooth muscle cells.¹⁴ Their intriguing results show that whereas most cells in the neointima are positive for -actin, desmin, and . . . [Full Text of this Article]

This article has been cited by other articles:

				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]

				P. F. Leite, A. Danilovic, P. Moriel, K. Dantas, S. Marklund, A. P. V. Dantas, and F. R.M. Laurindo Sustained Decrease in Superoxide Dismutase Activity Underlies Constrictive Remodeling After Balloon Injury in Rabbits Arterioscler Thromb Vasc Biol, December 1, 2003; 23(12): 2197 - 2202. [Abstract] [Full Text] [PDF]

				P. T. Nowicki, S. Flavahan, H. Hassanain, S. Mitra, S. Holland, P. J. Goldschmidt-Clermont, and N. A. Flavahan Redox Signaling of the Arteriolar Myogenic Response Circ. Res., July 20, 2001; 89(2): 114 - 116. [Abstract] [Full Text] [PDF]