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(Circulation Research. 2006;98:1453.)
© 2006 American Heart Association, Inc.

Editorials

Vascular Cell Locomotion

Osteopontin, NADPH Oxidase, and Matrix Metalloproteinase-9

Patrick J. Pagano, Mounir J. Haurani

From the Hypertension and Vascular Research Division (P.J.P.) and the Department of Surgery (M.J.H.), Henry Ford Research Institute and Hospital, Detroit, Mich.

Correspondence to Patrick J. Pagano, Hypertension and Vascular Research Division, Henry Ford Research Institute and Hospital, ER 7044; Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI 48202. E-mail PPAGANO1@hfhs.org

See related article, pages 1479–1489

Key Words: osteopontin • MMPs • superoxide • adventitia • myofibroblasts • neointima • vascular cell motility

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Since the discovery of osteopontin (OPN) in the vasculature, vascular biologists have been intrigued by its potential role in vascular arteriosclerosis and vessel calcification during the aging process.¹ Osteopontin is a phosphorylated acidic glycoprotein adhesion molecule, originally cloned from bone; and as in bone, its cardiovascular functions include cellular migration, adhesion, and spreading.² The most salient features of this intriguing calcium-regulating molecule are its ability to interact with _vß₃ and other integrins on the surface of cells. Because this ligand–receptor complex is known to be involved in cell migration, it is not surprising that an antibody to the ß₃ subunit of this receptor effectively reduced restenosis in patients.³ Interestingly, angiotensin II and other growth factors, including platelet-derived growth factor and transforming growth factor-ß, regulate OPN gene expression in vascular smooth muscle cell (VSMC) cultures and fibroblasts.^1,4 Cardiac fibroblasts have been extensively reported to produce OPN in response to these growth factors, resulting in fibroblast proliferation. On the one hand, OPN is thought to cause vascular dystrophy by altering extracellular matrix formation; on the other hand, cellular motogenesis is a hallmark of this emerging vascular cytokine. Its cellular expression includes a variety of inflammatory cells, such as T cells and macrophages, as well as mesenchymal cells of the vasculature including adventitial myofibroblasts. Moreover, OPN has both pro- and antiinflammatory properties. As a proinflammatory agent it can attract and modulate the function of the above mentioned cell types. Of seemingly major importance, OPN interacts with intracellular signaling agents to promote cell migration . . . [Full Text of this Article]

Related Article:

An Osteopontin–NADPH Oxidase Signaling Cascade Promotes Pro–Matrix Metalloproteinase 9 Activation in Aortic Mesenchymal Cells

Chung-Fang Lai, Venkat Seshadri, Kane Huang, Jian-Su Shao, Jun Cai, Radhika Vattikuti, Arwyn Schumacher, Arleen P. Loewy, David T. Denhardt, Susan R. Rittling, and Dwight A. Towler
Circ. Res. 2006 98: 1479-1489. [Abstract] [Full Text] [PDF]