Decreased plasma CXCL16/SR-PSOX concentration is associated with coronary artery disease
2006 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 188, no 2, 462-466 p.Article in journal (Refereed) Published
Objectives: To investigate for the first time whether the plasma CXCL16 concentration is altered in coronary artery disease (CAD) patients. Background: Accumulating evidence suggests that the novel chemokine/scavenger receptor CXCL16/SR-PSOX is involved in the development of atherosclerosis and CAD. Methods: Using ELISA we assessed the plasma CXCL16 concentration in 40 stable angina pectoris (SAP) patients, 17 unstable angina pectoris/non-ST-elevation myocardial infarction (UAP/non-STEMI) patients, 387 survivors of a first myocardial infarction (MI) and healthy control subjects (44 controls for SAP and UAP/non-STEMI patient groups and 387 controls for post-MI patients). Results: SAP patients exhibited significantly lower median CXCL16 levels (2111 pg/ml) than the corresponding control subjects (2678 pg/ml) (P = 0.0012). UAP/non-STEMI patients also appeared to have lower CXCL16 levels (2192 pg/ml) compared with controls (NS). Patients investigated 3 months after MI tended (P = 0.07) to have lower CXCL16 levels (2529 pg/ml) than the corresponding controls (2638 pg/ml). There were no significant correlations between CXCL16 levels and different measures of CAD severity determined by quantitative coronary angiography in post-MI patients. Neither patients nor controls exhibited significant correlations between CXCL16 levels and plasma lipoprotein fractions, inflammatory cytokines, C-reactive protein or numbers of inflammatory cells in peripheral blood. Conclusions: The finding that lower plasma CXCL16 concentration is associated with CAD might indicate a potential atheroprotective function of CXCL16. © 2005 Elsevier Ireland Ltd. All rights reserved.
Place, publisher, year, edition, pages
2006. Vol. 188, no 2, 462-466 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-34881DOI: 10.1016/j.atherosclerosis.2005.11.025Local ID: 23767OAI: oai:DiVA.org:liu-34881DiVA: diva2:255729