Inhibitors of Arterial Relaxation Among Components of Human Oxidized Low-Density Lipoproteins

Deckert, Valérie; Perségol, L.; Viens, Laura; Lizard, Gérard; Athias, Anne; Lallemant, Christian; Gambert, Philippe; Lagrost, Laurent

doi:10.1161/01.cir.95.3.723

Cited by 89 publications

(58 citation statements)

References 56 publications

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“…At the end, oxidation was stopped by adding EDTA (final concentration, 200 μmol/l) and butylated hydroxytoluene (final concentration, 20 μmol/l) and ox-LDL were kept at 4°C [9].…”

Section: Oxidative Modification Of Ldlmentioning

confidence: 99%

“…Vasoreactivity experiments were performed on rabbit (Charles River, L'Arbresle, France) aorta rings as previously described [9]. Our protocol has been approved by the local Ethics Committee for animals at Dijon University.…”

Section: Vasoreactivity On Rabbit Aorta Ringsmentioning

confidence: 99%

“…After wash-out and a 30-min recovery period, aortic rings were incubated for 2 h either with ox-LDL or HDL or both. The concentration of proteins in the organ bath (native or oxidised lipoproteins) was constantly 1 g/l for each lipoprotein subclass, as used in many previous studies conducted with rabbit aortic rings [5,9,12]. At the end of the incubation period, aortic segments were again contracted with arterenol hydrochloride and progressively relaxed with acetylcholine or with sodium nitroprussiate.…”

Section: Vasoreactivity On Rabbit Aorta Ringsmentioning

confidence: 99%

“…To test this hypothesis, we investigated whether HDL from type 2 diabetic patients show the same ability as HDL from normolipidaemic and normoglycaemic control subjects to protect endothelium-dependent vasorelaxation from the inhibitory effect of ox-LDL. In order to study the effect of HDL separately, our work was performed on isolated rings of rabbit aorta, a previously validated model [5,9]. In addition we measured the activity of paraoxonase (PON), an HDL-associated enzyme with an anti-oxidant role due to its ability to hydrolyse some oxidised lipids.…”

Section: Introductionmentioning

confidence: 99%

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Inability of HDL from type 2 diabetic patients to counteract the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation

et al. 2006

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Aims/hypothesis: In healthy normolipidaemic and normoglycaemic control subjects, HDL are able to reverse the inhibition of vasodilation that is induced by oxidised LDL. In type 2 diabetic patients, HDL are glycated and more triglyceride-rich than in control subjects. These alterations are likely to modify the capacity of HDL to reverse the inhibition of vasodilation induced by oxidised LDL. Subjects and methods: Using rabbit aorta rings, we compared the ability of HDL from 16 type 2 diabetic patients and 13 control subjects to suppress the inhibition of vasodilation that is induced by oxidised LDL. Results: Oxidised LDL inhibited endothelium-dependent vasodilation (maximal relaxation [Emax]=58.2± 14.6 vs 99.3±5.2% for incubation without any lipoprotein, p<0.0001). HDL from control subjects significantly reduced the inhibitory effect of oxidised LDL on vasodilatation (Emax=77.6±12.9 vs 59.5±7.7%, p<0.001), whereas HDL from type 2 diabetic patients had no effect (Emax=52.4±20.4 vs 57.2±18.7%, NS). HDL triglyceride content was significantly higher in type 2 diabetic patients than in control subjects (5.3±2.2 vs 3.1±1.4%, p<0.01) and was highly inversely correlated to Emax for oxidised LDL+HDL in type 2 diabetic patients (r=−0.71, p<0.005). Conclusions/interpretation: In type 2 diabetes mellitus, the ability of HDL to counteract the inhibition of endothelium-dependent vasorelaxation induced by oxidised LDL is impaired and is inversely correlated with HDL triglyceride content. These findings suggest that HDL are less atheroprotective in type 2 diabetic patients than in control subjects.

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“…At the end, oxidation was stopped by adding EDTA (final concentration, 200 μmol/l) and butylated hydroxytoluene (final concentration, 20 μmol/l) and ox-LDL were kept at 4°C [9].…”

Section: Oxidative Modification Of Ldlmentioning

confidence: 99%

Section: Vasoreactivity On Rabbit Aorta Ringsmentioning

confidence: 99%

Section: Vasoreactivity On Rabbit Aorta Ringsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inability of HDL from type 2 diabetic patients to counteract the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation

et al. 2006

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“…A cholesterol molecule may also be oxidized with the consequent formation of cholesterol oxides (oxysterols). Cholesterol oxized in position 7 may reduce endothelium-dependent relaxation and nitric oxide production by endothelial cells 20 . High concentrations of cholesterol oxides are found in atherosclerotic arteries and in lipoproteins of hypercholesterolemic patients 21 .…”

Section: Lipid Peroxidation and Nitric Oxide Inactivation In Postmenomentioning

confidence: 99%

Lipid peroxidation and nitric oxide inactivation in postmenopausal women

Pereira

Bertolami

Faludi

et al. 2003

Arq. Bras. Cardiol.

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Original ArticleCardiovascular diseases are less prevalent in premenopausal women and in those receiving hormone replacement therapy as compared with postmenopausal women and men 1 . This protective effect is attributed to estrogens, and one of the mechanisms of action may be related to the metabolism of plasma lipoproteins 2 .Estrogens reduce LDL-cholesterol and increase HDLcholesterol 3 . However, these changes in lipid profile only contribute to approximately 25% of the protective effect of estrogens 4 . Other potential mechanisms of action of estrogens may include protection against LDL oxidation 5 , reduction in lipoprotein(a), potentiation of fibrinolysis 6 , and increase in insulin sensitivity. In the arteries, estrogens improve vasodilating function, decrease calcification, secretion of cell adhesion molecules (E-selectin, ICAM-1, and VCAM-1), and formation of atherosclerotic lesions 7 .Direct action of estrogens on the arterial wall has also been demonstrated. The administration of estrogens for prolonged periods inhibits the deposition of cholesterol in the arteries and thickening of the intima in monkeys and rabbits fed an atherogenic diet 8 . However, the mechanisms determining the direct effects of estrogens on the arterial wall have not been completely elucidated. The hemodynamic effects may be partially measured by the activity of estrogens on the synthesis of endothelial nitric oxide 9 . Estrogens have been suggested to possibly improve endothelial function and decrease the risks of atherosclerosis in premenopausal women. Nitric oxide has its bioactivity reduced in postmenopausal women. However, it is not clear whether this occurs due to its lower production by nitric oxide synthase, or whether nitric oxide is inactivated by reaction with the superoxide radical also generated by endothelial cells, forming the peroxynitrite anion (ONOO -), which is a strong oxidizing agent.Peroxynitrite is decomposed into other reactive oxygen species ( fig. 1) 10 and reacts with tyrosine residues of proteins to form nitrotyrosine 11 . Although little is known NOx, nitrotyrosine, COx, CE 18:2 -OOH, and PC-OOH were higher in the postmenopausal period (33.8±22.3 µM; 230±130 nM; 55±19 ng/µL; 17±8.7 nM; 2775±460 nM, respectively) Objective -To assess the effect of endogenous estrogens on the bioavailability of nitric oxide (·NO) and in the formation of lipid peroxidation products in pre-and postmenopausal women. Methods -NOx and S-nitrosothiols were determined by gaseous phase chemiluminescence, nitrotyrosine was determined by ELISA, COx (cholesterol oxides) by gas chromatography, and cholesteryl linoleate hydroperoxides (CE 18:2 -OOH), trilinolein (TG 18:2 -OOH), and phospholipids (PC-OOH) by HPLC in samples of plasma. Results -The concentrations of

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Cellular toxicity of oxycholesterols

et al. 2006

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Oxycholesterols (OS) are formed from cholesterol or its immediate precursors by enzymatic or free radical action in vivo, or they may be derived from food. OS exhibit a wide spectrum of biological activities. In OS cytotoxicity, several mechanisms seem to be involved: e.g. inhibition of HMG-CoA reductase activity, antiproliferative action, apoptosis induction, replacement of cholesterol by OS in membranes followed by changes in cellular membrane structure and functionality, and immune system functions alteration. Furthermore, OS may be mutagenic and carcinogenic and may serve as intracellular signaling or regulatory molecules. Here we review OS cellular activities with special attention to the cytotoxic action in vivo and in vitro using experimental models.

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Inhibitors of Arterial Relaxation Among Components of Human Oxidized Low-Density Lipoproteins

Abstract: Cholesterol derivatives in oxidized LDL can reduce maximal arterial relaxation through a specific effect on vascular endothelial cells.

Cited by 89 publications

References 56 publications

Inability of HDL from type 2 diabetic patients to counteract the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation

Inability of HDL from type 2 diabetic patients to counteract the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation

Lipid peroxidation and nitric oxide inactivation in postmenopausal women

Cellular toxicity of oxycholesterols

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