Low Density Lipoprotein-Apheresis Decreases Oxidized Low Density Lipoproteins and Monocyte Adhesion to Endothelial Cells

Cattin, Luigi; Petrucco, A.; Cazzolato, G.; Bon, Gabriele Bittolo; Borelli, Violetta; Nardon, Ermanno; Zabucchi, Giuliano; Fonda, M.; Bordin, Paolo

doi:10.1097/00002480-199743030-00016

Cited by 7 publications

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“…51 After LDL apheresis, the endothelium-dependent vasodilation was found to be ameliorated, 12,52,53 and the adhesion of monocytes to the endothelium was observed to be diminished. 13,14 On the basis of the results of the present study, these earlier findings might be partially explained by the diminished lysoPC contents of the particles ( Table 2). The reasons for the increased PC/ lysoPC ratios after apheresis are unknown.…”

Section: Discussionsupporting

confidence: 67%

“…12 The procedure also led to diminished expression of endothelial adhesion molecules. 13,14 Thus, typical proatherogenic consequences of oxidized LDL are attenuated after therapeutic reduction of LDL. Although removal of the particles per se might partially account for these effects, changes in the oxidizability of the LDL induced by LDL apheresis could also be relevant.…”

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confidence: 99%

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Role of Plasmalogens in the Enhanced Resistance of LDL to Copper-Induced Oxidation After LDL Apheresis

Hahnel¹,

Thiery²,

Brosche³

et al. 1999

ATVB

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Extracorporeal reduction of plasma low density lipoproteins (LDLs) by LDL apheresis was shown to attenuate the proatherogenic influences of LDL, such as impairment of vasodilation and increased monocyte adhesion to the endothelium. In 16 patients with familial hypercholesterolemia, we analyzed whether LDL apheresis by the heparin precipitation procedure affected the oxidative resistance of LDL. Plasma LDL cholesterol concentrations were reduced by 65% after the apheresis. The lag time of copper-mediated LDL oxidation was increased from 103 to 117 minutes (P<0.0005). The LDL contents of alpha-tocopherol and beta-carotene, as well as the ratio of monounsaturated to polyunsaturated fatty acids in LDL, were not altered. However, the LDL apheresis induced a 15% increase in the LDL contents of plasmalogen phospholipids (P<0.0005), a class of ether phospholipids that were recently shown to prevent lipid oxidation. The phosphatidylcholine (PC) to lysoPC ratio was elevated by 16% after the apheresis (P<0.0005). The percent increase in LDL plasmalogen phospholipids showed a close association with the increased lag time after apheresis (P<0.0005). The LDL plasmalogen contents of the blood samples from patients and from normolipidemic donors were also positively related to the lag time (P<0.005). In vitro loading of LDL with plasmalogen phospholipids resulted in a prolongation of the lag time and an increase in the PC/lysoPC ratio. In conclusion, the rapid rise in LDL contents of plasmalogen phospholipids most probably causes the increase in lag time after LDL apheresis. Plasmalogens appear to play an important role in the oxidation resistance of LDL in vivo.

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Section: Discussionsupporting

confidence: 67%

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confidence: 99%

Role of Plasmalogens in the Enhanced Resistance of LDL to Copper-Induced Oxidation After LDL Apheresis

Hahnel¹,

Thiery²,

Brosche³

et al. 1999

ATVB

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“…Such a finding could be the effect of an increase in the activities of free radical scavenging enzymes in erythrocytes, as observed by Schettler et al [10,37] during regular LDL-apheresis by the HELP technique. On the other hand, other antioxidant factors, such as the lipophilic vitamins α-tocopherol and β-carotene, and the plasmalogen content of plasma phospholipids, have been reported previously to increase the resistance of LDL to oxidation [35,38,40,41]. On the other hand, other antioxidant factors, such as the lipophilic vitamins α-tocopherol and β-carotene, and the plasmalogen content of plasma phospholipids, have been reported previously to increase the resistance of LDL to oxidation [35,38,40,41].…”

Section: Discussionmentioning

confidence: 98%

“…This effect is probably mediated by the removal of the LDL particles that are more susceptible to oxidation, such as the small dense LDL subfraction present in high amounts in individuals predisposed to coronary artery disease [35,36]. samples -seems to demonstrate that the treatment has an antioxidative effect.…”

Section: Discussionmentioning

confidence: 99%

Acute and long-term effects of low-density lipoprotein (LDL)-apheresis on oxidative damage to LDL and reducing capacity of erythrocytes in patients with severe familial hypercholesterolaemia

et al. 2001

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Several studies have suggested that the oxidative modification of low-density lipoprotein (LDL) could play a key role in the early stages of atherosclerosis. The susceptibility of LDL to oxidation has been found to be greater in patients with coronary heart disease. Familial hypercholesterolaemia (FH) is a powerful clinical model in which to study the predictive role of LDL in atherogenesis. LDL-apheresis is a treatment that is able to decrease lipid levels in plasma. This study was aimed at investigating the reducing capacity of erythrocytes and the in vitro susceptibility to oxidation of LDL isolated from patients with homozygous, heterozygous and double-heterozygous FH, who were treated fortnightly with LDL-apheresis or left untreated. In 14 FH patients, at baseline and after a cycle of treatment, the susceptibility of LDL to oxidative modification was analysed by studying the kinetics of conjugate diene formation. Plasma hydroperoxides, polyunsaturated fatty acid content, LDL electrophoretic mobility on agarose, the titre of auto-antibodies against oxidized LDL and serum paraoxonase activity were also measured. Furthermore, in order to evaluate a potential relationship between LDL oxidation and redox status, erythrocyte GSH and ATP levels were determined in FH patients treated regularly or never treated previously by LDL-apheresis. Unlike in the control group, the oxidative status of LDL in all FH patients was modified by LDL-apheresis, as revealed by the higher negative charge and the increase in levels of hydroperoxides and antibodies against oxidized LDL in the plasma. Our findings suggest both an acute effect and a long-term effect of LDL-apheresis in FH patients treated with dextran sulphate cellulose apheresis. The acute effect of LDL-apheresis on the susceptibility to oxidation of plasma and LDL was demonstrated by significant decreases in plasma hydroperoxide content, total LDL concentration and polyunsaturated fatty acid content. The increased resistance of LDL to oxidation was shown by prolongation of the lag time (P<0.05) in samples after a single cycle of treatment. The long-term effect of LDL-apheresis was demonstrated by the comparable values for lag phases (obtained from the kinetics of conjugate diene formation) in patients under active treatment and controls. Compared with healthy controls and untreated patients, the erythrocyte GSH content was significantly higher (P

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“…Mononuclear cells exposed to oxidized LDL-cholcsterol species secrete factors that stimulate endothelial cells to express monocytes adhesion molecules and to produce monocyte chemotactie factors (40). LDL-cholesterol decrease, caused by LDL-apheresis, is accompanied by a reduction of monocyte adhesion to endothelial cells (41 ). Reduction of plasma concentrations of soluble leukocyte adhesion and chemotactic molecules was observed after a single procedure using different LDL-apheresis methods (42,43,44).…”

Section: Discussionmentioning

confidence: 99%

Urinary Neopterin and Microalbuminuria in Patients Treated by Low-density Lipoprotein Apheresis

Cermanová¹,

Melichar²,

Solichová³

et al. 2005

Pteridines

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ΊΙ. Interni klinika,; Klinika onkologie a radioterapie, -'Klinika gerontologická a metabolická, 4 Katedra lékarské biofyziky, Lékarská fakulta University Karlovy a Fakultní nemocnice Hradee Králové, Czech republic. AbstractLow-density lipoprotein (LDL)-apheresis is a method of extracorporeal elimination of LDL-cholesterol in patients with severe primary lipoprotein disorders. LDL-cholesterol activates macrophages, which play an important role in atheromatous plaque formation. In the present study, we have investigated urinary neopterin, a specific marker of macrophage activation and microalbuminuria, an indicator of generalized vascular dysfunction, after a single LDL-apheresis procedure in 10 patients with severe primary lipoprotein disorder. The urinary neopterin/creatinine ratio was increased in patients compared to controls. No significant changes of the neopterin/creatinine and albumin/creatinine ratios were observed after LDL-apheresis, except a significant (p < 0.006) decrease of urinary neopterin/creatinine ratio in the evening after the apheresis. This decrease showed significant negative correlation with the pre-apheretic levels of atherogenic cholesterol fractions (p < 0.05) and with cholesterol decrease during the apheresis (p < 0.05). Urinary albumin/creatinine ratio correlated positively with total and LDL-cholesterol levels before the apheresis and with the evening urinary neopterin/creatinine ratio after the apheresis, but did not correlate with glycemia and triacylglycerides. Elevated urinary neopterin in the patients with severe primary lipoprotein disorders reflects the presence of atherosclerosis. A single LDL-apheresis procedure did not significantly affect microalbuminuria. The decrease of urinary neopterin in the evening after the apheresis corresponds with the diurnal rhythm of neopterin excretion and was less pronounced in patients with more severe hypercholesterolemia. The correlations between microalbuminuria, neopterin and pre-apheretic cholesterol concentrations indicate a possible connection between microvascular dysfunction, macrophage activity and severity of hyperlipidemia, but these results should be interpreted with caution because of small number of subjects evaluated.

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Low Density Lipoprotein-Apheresis Decreases Oxidized Low Density Lipoproteins and Monocyte Adhesion to Endothelial Cells

Cited by 7 publications

References 0 publications

Role of Plasmalogens in the Enhanced Resistance of LDL to Copper-Induced Oxidation After LDL Apheresis

Role of Plasmalogens in the Enhanced Resistance of LDL to Copper-Induced Oxidation After LDL Apheresis

Acute and long-term effects of low-density lipoprotein (LDL)-apheresis on oxidative damage to LDL and reducing capacity of erythrocytes in patients with severe familial hypercholesterolaemia

Urinary Neopterin and Microalbuminuria in Patients Treated by Low-density Lipoprotein Apheresis

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