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Sökning: WFRF:(Sheikine Y)

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  • Olofsson, P. S., et al. (författare)
  • A functional interleukin-1 receptor antagonist polymorphism influences atherosclerosis development - The interleukin-1β : Interleukin-1 receptor antagonist balance in atherosclerosis
  • 2009
  • Ingår i: Circulation Journal. - : Japanese Circulation Society,Nihon Junkanki Gakkai. - 1346-9843 .- 1347-4820. ; 73:8, s. 1531-1536
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Interleukin (JL)-β plays a central role in inflammation and atherosclerosis, but levels of IL-1β, its natural antagonist, IL-1Ra, and their balance in human atherosclerotic lesions, are unknown. Knowledge of protein levels in atherosclerosis and the influence of a functional IL-1Rα polymorphism would increase the understanding of atherosclerosis pathogenesis.Methods and Results: Fresh and endotoxin-stimulated explanted human atherosclerotic and normal arteries were analyzed for IL-1β, IL-1Ra and IL-1 receptor 1 (IL-1R1) using TaqMan PCR and enzyme-linked immunosorbent assay. Two hundred forty-three survivors of a first myocardial infarction were genotyped for a polymorphism in IL-1Ra and their coronary atherosclerosis analyzed by using coronary angiography. Levels of IL-1β, IL-1Ra and IL-1R1 mRNA were significantly increased in atherosclerotic arteries compared with normal arteries. Endotoxin stimulation increased IL-1β levels more than IL-1Ra levels (ie, promoted a pro-inflammatory state). A polymorphism in IL-1Ra known to increase levels of IL-1Ra was associated with decreased mean coronary artery plaque area.Conclusions: Activation of innate immunity changed the balance between IL-1β and IL-1Ra in atherosclerotic arteries towards a more pro-inflammatory state. In line with this, the presence of an IL-1Ra intron 2 polymorphism known to increase IL-1Ra levels, and possibly the IL-1Ra:IL-1β ratio, was associated with reduced coronary atherosclerosis.
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  • Sheikine, Y, et al. (författare)
  • Chemokines and atherosclerosis
  • 2004
  • Ingår i: Annals of medicine. - : Informa UK Limited. - 0785-3890 .- 1365-2060. ; 36:2, s. 98-118
  • Tidskriftsartikel (refereegranskat)
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  • Sheikine, Y, et al. (författare)
  • Decreased plasma CXCL16/SR-PSOX concentration is associated with coronary artery disease
  • 2006
  • Ingår i: Atherosclerosis. - : Elsevier BV. - 0021-9150 .- 1879-1484. ; 188:2, s. 462-466
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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