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 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 Cybulsky, M. I. Search for Related Content PubMed Articles by Cybulsky, M. I. Related Collections Related Articles

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1887.)
© 2008 American Heart Association, Inc.

Editorials

Morphing the Topography of Atherosclerosis

An Unexpected Role for PECAM-1

Myron I. Cybulsky

From the Toronto General Research Institute, University Health Network and the Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.

Correspondence to Dr Myron Cybulsky, University Health Network, 200 Elizabeth Street, Eaton 11, Toronto ON M5G 2C4, Canada. E-mail myron.cybulsky@utoronto.ca

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

Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) is a complex adhesion and signaling molecule expressed by endothelial cells, platelets, and leukocytes.^1,2 On endothelial cells this transmembrane glycoprotein member of the immunoglobulin gene superfamily is concentrated at intercellular junctions and cycles through vesicle-like structures contiguous with the lateral plasma membrane, termed the lateral border recycling compartment.³ Homophilic adhesive interactions between PECAM-1 on leukocytes and endothelial cells mediate leukocyte migration through endothelial cell monolayers (diapedesis) in vitro and in vivo and through the perivascular basement membrane.^2,4 As a signaling molecule, PECAM-1 transduces signals required for proinflammatory adhesion molecule expression by endothelial cells. However, PECAM-1 can also inhibit inflammatory and immune responses.² Thus, PECAM-1 has the potential to influence atherogenesis in more than one way.

See accompanying articles on pages 1996 and 2003

Usually the deficiency of a molecule leads to an overall increase, decrease, or no change in murine atherosclerotic lesion burden, but the distribution of lesions in the arterial tree remains unchanged, with the majority of lesions occurring in the aortic root, the lesser (inner) curvature of the ascending aorta and near ostia of arterial branches in the descending aorta.⁵ In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, two articles detail independent obserations that deficiency of PECAM-1 results in an altered distribution of atherosclerotic lesions.

Goel et al⁶ evaluated atherosclerotic lesion development in LDL receptor deficient (ldlr^–/–) mice by measuring lipid accumulation using oil red O staining in en face preparations of the aorta and cross-sections of . . . [Full Text of this Article]

Related Articles:

Endothelial Cell PECAM-1 Promotes Atherosclerotic Lesions in Areas of Disturbed Flow in ApoE-Deficient Mice

Brian L. Harry, John M. Sanders, Ryan E. Feaver, Melissa Lansey, Tracy L. Deem, Alexander Zarbock, Anthony C. Bruce, Andrew W. Pryor, Bradley D. Gelfand, Brett R. Blackman, Martin A. Schwartz, and Klaus Ley
Arterioscler Thromb Vasc Biol 2008 28: 2003-2008. [Abstract] [Full Text] [PDF]

Site-Specific Effects of PECAM-1 on Atherosclerosis in LDL Receptor–Deficient Mice

Reema Goel, Benjamin R. Schrank, Shikha Arora, Brian Boylan, Barbara Fleming, Hiroto Miura, Peter J. Newman, Robert C. Molthen, and Debra K. Newman
Arterioscler Thromb Vasc Biol 2008 28: 1996-2002. [Abstract] [Full Text] [PDF]