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      Interaction between C-Reactive Protein and Endothelin-1 in Coronary Artery Disease


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          Background: Increased concentrations of serum C-reactive protein (CRP) have been reported to predict major cardiovascular events in patients with coronary artery disease (CAD). Increased concentrations of endothelin-1 (ET-1) are also associated with poor prognosis after myocardial infarction. Hypothesis: We tested the hypothesis that ET-1 might contribute to CRP in prediction of adverse outcome in CAD. Methods: Serum high sensitive CRP and plasma ET-1 levels of 40 patients who have stable CAD and 25 control subjects were measured, and correlation analysis between these molecules was performed. Results: Mean high sensitive CRP was 8.64 ± 12.73 mg/l, and mean ET-1 was 8.24 ± 7.06 pg/ml in the CAD group. We found that there was no statistically significant correlation between high sensitive CRP and ET-1 in either CAD group (p = 0.82), or the control group (p = 0.85). In a subgroup of 13 patients who were not under statin treatment, we found a strong correlation between the levels of these molecules (p = 0.01). Conclusion: Our study does not clearly support or exclude a link between CRP and ET-1 in patients who have stable CAD.

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          Most cited references 8

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          Production of C-reactive protein and risk of coronary events in stable and unstable angina

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            Endothelin antagonism and interleukin-6 inhibition attenuate the proatherogenic effects of C-reactive protein.

            C-reactive protein (CRP) has been suggested to actively participate in the development of atherosclerosis. In the present study, we examined the role of the potent endothelium-derived vasoactive factor endothelin-1 (ET-1) and the inflammatory cytokine interleukin-6 (IL-6) as mediators of CRP-induced proatherogenic processes. Saphenous vein endothelial cells (HSVECs) were incubated with human recombinant CRP (25 microg/mL, 24 hours) and the expression of vascular cell adhesion molecule (VCAM-1), intracellular adhesion molecule (ICAM-1), and monocyte chemoattractant chemokine-1 was determined. The effects of CRP on LDL uptake were assessed in macrophages using immunofluorescent labeling of CD32 and CD14. In each study, the effect of endothelin antagonism (bosentan) and IL-6 inhibition (monoclonal anti-IL-6 antibodies) was examined. The effects of CRP on the secretion of ET-1 and IL-6 from HSVECs were also evaluated. Incubation of HSVECs with recombinant human CRP resulted in a marked increase in ICAM-1 and VCAM-1 expression (P<0.001). Likewise, CRP caused a significant increase in monocyte chemoattractant chemokine-1 production, a key mediator of leukocyte transmigration (P<0.001). CRP caused a marked and sustained increase in native LDL uptake by macrophages (P<0.05). These proatherosclerotic effects of CRP were mediated, in part, via increased secretion of ET-1 and IL-6 (P<0.01) and were attenuated by both bosentan and IL-6 antagonism (P<0.01). CRP actively promotes a proatherosclerotic and proinflammatory phenotype. These effects are mediated, in part, via the production of ET-1 and IL-6 and are attenuated by mixed ET(A/B) receptor antagonism and IL-6 inhibition. Bosentan may be useful in decreasing CRP-mediated vascular disease.
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              Effects of the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, atorvastatin and simvastatin, on the expression of endothelin-1 and endothelial nitric oxide synthase in vascular endothelial cells.

              Endothelial dysfunction associated with atherosclerosis has been attributed to alterations in the L-arginine-nitric oxide (NO)-cGMP pathway or to an excess of endothelin-1 (ET-1). The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been shown to ameliorate endothelial function. However, the physiological basis of this observation is largely unknown. We investigated the effects of Atorvastatin and Simvastatin on the pre-proET-1 mRNA expression and ET-1 synthesis and on the endothelial NO synthase (eNOS) transcript and protein levels in bovine aortic endothelial cells. These agents inhibited pre-proET-1 mRNA expression in a concentration- and time-dependent fashion (60-70% maximum inhibition) and reduced immunoreactive ET-1 levels (25-50%). This inhibitory effect was maintained in the presence of oxidized LDL (1-50 microg/ml). No significant modification of pre-proET-1 mRNA half-life was observed. In addition, mevalonate, but not cholesterol, reversed the statin-mediated decrease of pre-proET-1 mRNA levels. eNOS mRNA expression was reduced by oxidized LDL in a dose-dependent fashion (up to 57% inhibition), whereas native LDL had no effect. Statins were able to prevent the inhibitory action exerted by oxidized LDL on eNOS mRNA and protein levels. Hence, these drugs might influence vascular tone by modulating the expression of endothelial vasoactive factors.

                Author and article information

                S. Karger AG
                May 2007
                01 February 2007
                : 107
                : 4
                : 340-344
                Marmara University School of Medicine, Istanbul, Turkey
                99048 Cardiology 2007;107:340–344
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 3, References: 25, Pages: 5
                Original Research


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