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      Serum Neutrophil Gelatinase-Associated Lipocalin Levels and Aortic Stiffness in Noncritical Coronary Artery Disease

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          Aim: The aim of this study was to establish the degree of aortic stiffness and levels of neutrophil gelatinase-associated lipocalin (NGAL) in patients with stable ischemic heart disease. Materials and Methods: Patients who were found to have stable, noncritical lesions on coronary angiography were included in the study [noncritical coronary artery disease (CAD)]. The control group consisted of those patients who had similar risk profiles and metabolic parameters without atherosclerosis on angiography. Results: A total of 101 patients were included in the study of which 56 had noncritical CAD. Whereas the aortic strain (9.11 ± 3.4 vs. 14.01 ± 4.1%, p < 0.001) and aortic distensibility (3.98 ± 1.9 10<sup>-6</sup> cm<sup>2</sup>/dyn vs. 6.33 ± 2.3 10<sup>-6</sup> cm<sup>2</sup>/dyn, p < 0.001) were lower in the noncritical CAD group, the aortic stiffness index was higher (6.34 ± 3.9 vs. 3.37 ± 2.4, p < 0.001) as compared to controls. Serum NGAL levels were higher in the noncritical CAD group (79.29 ± 38.8 vs. 48.05 ± 21.4 ng/ml, p < 0.001). NGAL levels were negatively correlated with aortic strain (p < 0.01, r = 0.57) and distensibility (p < 0.001, r = 0.62), but positively correlated with the aortic stiffness index (p < 0.001, r = 0.72). Conclusion: We show that in patients with noncritical CAD, the degree of aortic stiffness and NGAL levels are higher. These markers can be used as tools for further risk stratification of patients with noncritical CAD.

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          Most cited references 23

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          Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries.

           L Ludmer,  R Wayne,  G Mudge (1986)
          Acetylcholine is believed to dilate normal blood vessels by promoting the release of a vasorelaxant substance from the endothelium (endothelium-derived relaxing factor). By contrast, if the endothelium is removed experimentally, acetylcholine constricts blood vessels. We tested the hypothesis that muscarinic cholinergic vasodilation is impaired in coronary atherosclerosis. Graded concentrations of acetylcholine and, for comparison, the nonendothelial-dependent vasodilator nitroglycerin were infused into the left anterior descending artery of eight patients with advanced coronary stenoses (greater than 50 percent narrowing), four subjects with angiographically normal coronary arteries, and six patients with mild coronary atherosclerosis (less than 20 percent narrowing). Vascular responses were evaluated by quantitative angiography. In several segments each of four normal coronary arteries, acetylcholine caused a dose-dependent dilation from a control diameter of 1.94 +/- 0.16 mm to 2.16 +/- 0.15 mm with the maximal acetylcholine dose (P less than 0.01). In contrast, all eight of the arteries with advanced stenoses showed dose-dependent constriction, from 1.05 +/- 0.05 to 0.32 +/- 0.16 mm at the highest concentration of acetylcholine (P less than 0.01), with temporary occlusion in five. Five of six vessels with minimal disease also constricted in response to acetylcholine. All vessels dilated in response to nitroglycerin, however. We conclude that paradoxical vasoconstriction induced by acetylcholine occurs early as well as late in the course of coronary atherosclerosis. Our preliminary findings suggest that the abnormal vascular response to acetylcholine may represent a defect in endothelial vasodilator function, and may be important in the pathogenesis of coronary vasospasm.
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            The high molecular weight urinary matrix metalloproteinase (MMP) activity is a complex of gelatinase B/MMP-9 and neutrophil gelatinase-associated lipocalin (NGAL). Modulation of MMP-9 activity by NGAL.

            Detection of matrix metalloproteinase (MMP) activities in the urine from patients with a variety of cancers has been closely correlated to disease status. Among these activities, the presence of a group of high molecular weight (HMW) MMPs independently serves as a multivariate predictor of the metastatic phenotype (). The identity of these HMW MMP activities has remained unknown despite their novelty and their potentially important applications in non-invasive cancer diagnosis and/or prognosis. Here, we report the identification of one of these HMW urinary MMPs of approximately 125-kDa as being a complex of gelatinase B (MMP-9) and neutrophil gelatinase-associated lipocalin (NGAL). Multiple biochemical approaches verified this identity. Analysis using substrate gel electrophoresis demonstrated that the 125-kDa urinary MMP activity co-migrates with purified human neutrophil MMP-9 x NGAL complex. The 125-kDa urinary MMP-9 x NGAL complex was recognized by a purified antibody against human NGAL as well as by a monospecific anti-human MMP-9 antibody. Furthermore, these same two antibodies were independently capable of specifically immunoprecipitating the 125-kDa urinary MMP activity in a dose-dependent manner. In addition, the complex of MMP-9 x NGAL could be reconstituted in vitro by mixing MMP-9 and NGAL in gelatinase buffers with pH values in the range of urine and in normal urine as well. Finally, the biochemical consequences of the NGAL and MMP-9 interaction were investigated both in vitro using recombinant human NGAL and MMP-9 and in cell culture by overexpressing NGAL in human breast carcinoma cells. Our data demonstrate that NGAL is capable of protecting MMP-9 from degradation in a dose-dependent manner and thereby preserving MMP-9 enzymatic activity. In summary, this study identifies the 125-kDa urinary gelatinase as being a complex of MMP-9 and NGAL and provides evidence that NGAL modulates MMP-9 activity by protecting it from degradation.
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              Prevention of dementia in randomised double-blind placebo-controlled Systolic Hypertension in Europe (Syst-Eur) trial


                Author and article information

                Cardiorenal Med
                Cardiorenal Medicine
                S. Karger AG
                December 2014
                18 July 2014
                : 4
                : 3-4
                : 147-154
                Departments of aCardiology and bRadiology, Faculty of Medicine, Ondokuz Mayis University, and cDepartment of Cardiology, Gazi State Hospital, Samsun, Departments of dCardiology and eBiochemistry, Aksaray State Hospital, Aksaray, and fDepartment of Cardiology, Artvin State Hospital, Artvin, Turkey
                Author notes
                *Korhan Soylu, MD, Department of Cardiology, Faculty of Medicine, Ondokuz Mayis University, TR-55139 Samsun (Turkey), E-Mail
                365200 PMC4299284 Cardiorenal Med 2014;4:147-154
                © 2014 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 2, Pages: 8
                Original Paper


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