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Circulation. 1997;95:1986-1988

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(Circulation. 1997;95:1986-1988.)
© 1997 American Heart Association, Inc.


Articles

Potential Significance of Circulating E-Selectin

C. Wayne Smith, MD

From the Section of Leukocyte Biology, Departments of Pediatrics and Microbiology and Immunology, Baylor College of Medicine, Houston, Tex.

Correspondence to C. Wayne Smith, MD, Leukocyte Biology Section, Clinical Care Center, Suite 1130, 6621 Fannin, MC 3-2372, Houston, TX 77030-2399. E-mail cwsmith@bcm.tmc.edu


Key Words: Editorials • leukocytes • restenosis


*    Introduction
 
In the accompanying article, Belch and colleagues1 propose a model in which baseline levels of serum E-selectin (CD62E) are predictive of restenosis after percutaneous transluminal angioplasty in patients with peripheral arterial occlusive disease. Their data revealed significantly higher baseline serum E-selectin levels in patients who restenosed compared with those who did not. The source of the circulating soluble E-selectin in these patients was not revealed, but other studies have shown E-selectin to be expressed on luminal arterial endothelial cells, neovasculature, and adventitial vasa vasorum associated with atherosclerotic lesions.2 3 4 In these reports, the luminal E-selectin was increased in arterial segments with mononuclear cell infiltration. Extensive immunohistological examinations of a wide variety of tissues and inflammatory lesions have revealed two important features regarding E-selectin expression. It is generally absent in normal tissues,5 6 7 and E-selectin has not been seen on cells other than endothelium. While direct demonstration of endothelium as the source of circulating E-selectin has not been accomplished, in vitro studies have shown that human umbilical vein endothelial cells stimulated with interleukin-1ß, tissue necrosis factor-{alpha}, or endotoxin will release E-selectin into the culture supernate,8 9 10 and this soluble E-selectin is 5 to 7 kD smaller than that obtained by detergent extraction of the stimulated endothelial cells. E-selectin found in human serum also has a lower apparent molecular weight and appears to lack the cytoplasmic domain.10 The most likely hypothesis is that plasma E-selectin results from proteolytic cleavage of endothelial E-selectin expressed after cytokine stimulation.11

Elevations of soluble E-selectin have been reported in . . . [Full Text of this Article]




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