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This Article Full Text Full Text (PDF) All Versions of this Article: clinchem.2009.125518v1 55/6/1051    most recent Alert me when this article is cited Alert me if a correction is posted 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 Google Scholar Articles by Chasman, D. I. Articles by Paré, G. PubMed PubMed Citation Articles by Chasman, D. I. Articles by Paré, G.

Getting Closer to P-Selectin

¹ Brigham and Women's Hospital and Harvard Medical School, Boston, MA.

^aAddress correspondence to this author at: Brigham and Women's Hospital and Harvard Medical School, 900 Commonwealth Avenue, East, 02215, Boston, MA. Fax 617-232-3541; e-mail dchasman@rics.bwh.harvard.edu.

The first 20% of the full text of this article appears below.

Inflammation is recognized for its important role in the pathophysiology of atherosclerosis (1). However, the use of genetic association studies to dissect the impact of inflammatory genes on vascular disease is challenging because of the relatively small effects expected for common variants and the difficulty of identifying surrogates that best reflect underlying disease processes. In this issue of Clinical Chemistry, Volcik and colleagues (2) suggest an original design to address these issues by looking for genetic associations with the cell-surface concentration of a pair of cognate cell-surface receptors, P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1).¹ P-selectin [encoded by the selectin P (granule membrane protein 140kDa, antigen CD62) (SELP) gene² ] is primarily stored in platelets and endothelial cells, but it translocates to the cell surface upon activation and binding to its counterreceptor PSGL-1 [encoded by the selectin P ligand (SELPLG) gene] located on leukocytes. Adhesion of leukocytes to endothelium, with subsequent migration into the vascular wall, similarly involves P-selectin interaction with PSGL-1. Thus, the P-selectin–PSGL-1 interaction is thought to be of central importance in thrombosis, hemostasis, and vascular inflammation. A role for the P-selectin system in atherogenesis is indicated by decreased atherosclerotic plaques among apolipoprotein E (APOE –/–) mice also deficient in either platelet or endothelial P-selectin (3). More . . . [Full Text of this Article]