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 Google Scholar Google Scholar Articles by Shaheen, M. Articles by Weintraub, N. L. Search for Related Content PubMed PubMed Citation Articles by Shaheen, M. Articles by Weintraub, N. L. Related Collections Related Article

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:439.)
© 2007 American Heart Association, Inc.

Editorials

Osteopontin

A Bona Fide Mediator of Abdominal Aortic Aneurysm?

Mazen Shaheen; Neal L. Weintraub

From the Department of Internal Medicine, Cardiovascular Division, University of Cincinnati College of Medicine, Cincinnati, Ohio, and Research Service, Veteran’s Administration Medical Center, Cincinnati, Ohio.

Correspondence to Dr Neal L. Weintraub, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Cincinnati College of Medicine, 231 Albert Sabin Way, ML 0542, MSB 3363, PO Box 670542, Cincinnati, Ohio 45267-0542. E-mail neal.weintraub@uc.edu

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

Osteopontin is an arginine-glycine–aspartate (RGD) containing adhesive glycoprotein first identified in bone but subsequently detected in many other tissues, including, dentin, cartilage, kidney, and vascular tissues.^1–3 It is expressed by a wide variety of inflammatory cells (eg, macrophages, T lymphocytes, NK cells), and, to a lesser extent, by endothelial cells and smooth muscle cells. The RGD domain facilitates tissue binding of osteopontin to various extracellular matrix proteins, such as _vß₃ integrin and fibronectin. Additionally, osteopontin may engage CD44 through an RGD-independent mechanism. In extracellular fluids, osteopontin functions as a cytokine, and its plasma levels are increased in autoimmune diseases such as lupus, rheumatoid arthritis, and multiple sclerosis.⁴ The diverse biological actions of osteopontin could potentially regulate many processes pertinent to vascular disease, including inflammation, cell adhesion, viability, angiogenesis, and calcification (Figure).^5,6 Such actions may underlie its presumed role in the pathophysiology of atherosclerosis and in modulating arteriopathy associated with diabetes and chronic renal failure (reviewed by Johnson et al⁷). Of relevance to the present topic, Bruemmer et al reported that deletion of osteopontin reduced formation of abdominal aortic aneurysms (AAA) in mice infused with angiotensin II.⁸

View larger version (35K):   Overview of potential mechanisms whereby osteopontin may bind to extracellular matrix proteins (eg, integrin) and adhesion molecules (eg, CD44) to regulate vascular disease.

See page 655

Conceptually, it is logical to presume that osteopontin would contribute to the pathogenesis of AAA. First, in experimental models and in humans, AAA are characterized by extensive inflammatory cell infiltration and induction of proinflammatory cytokines.^9–12 . . . [Full Text of this Article]

Related Article:

Association Between Osteopontin and Human Abdominal Aortic Aneurysm

Jonathan Golledge, Juanita Muller, Neil Shephard, Paula Clancy, Linda Smallwood, Corey Moran, Anthony E. Dear, Lyle J. Palmer, and Paul E. Norman
Arterioscler Thromb Vasc Biol 2007 27: 655-660. [Abstract] [Full Text] [PDF]