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This Article Full Text Full Text (PDF) All Versions of this Article: 93/9/1085    most recent expphysiol.2008.042267v1 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 Brinkley, T. E. Articles by Hagberg, J. M. PubMed PubMed Citation Articles by Brinkley, T. E. Articles by Hagberg, J. M. Related Collections Vascular

¹ Department of Kinesiology, University of Maryland, College Park, MD 20742, USA ² Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan ³ Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA

The lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) expressed on vascular cells plays a major role in atherogenesis by internalizing and degrading oxidized low-density lipoprotein. LOX-1 can be cleaved from the cell surface and released as soluble LOX-1 (sLOX-1), and elevated sLOX-1 levels may be indicative of atherosclerotic plaque instability. We examined associations between the LOX-1 gene 3'UTR-C/T and G501C polymorphisms and plasma sLOX-1 levels in 97 healthy older men and women. The frequencies for the 3'UTR-T and 501C alleles were 46 and 10%, respectively. Plasma sLOX-1 levels were significantly higher in the 3'UTR CC genotype group compared with both the CT (P = 0.02) and TT genotype groups (P = 0.002). Plasma sLOX-1 levels were also significantly higher in the 501GC genotype group compared with the GG genotype group (P = 0.004). In univariate analyses, sLOX-1 levels were significantly associated with both the 3'UTR-C/T and G501C polymorphisms. These associations remained significant after adjusting for age, sex, race and body mass index. In conclusion, variation in the LOX-1 gene is associated with plasma sLOX-1 levels in older men and women.

(Received 11 February 2008; accepted after revision 6 May 2008; first published online 9 May 2008)
Corresponding author T. E. Brinkley: Department of Internal Medicine, Section on Gerontology and Geriatric Medicine, Wake Forest University Health Sciences, Winston-Salem, NC 27157, USA. Email: tiellis{at}wfubmc.edu