Increased Plasma and Lipoprotein Lipid Peroxidation in apo E-Deficient Mice

Hayek, Tony; Oiknine, J.; Brook, J.G.; Aviram, Michael

doi:10.1006/bbrc.1994.1883

Cited by 168 publications

(107 citation statements)

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“…2). These observations would support previous suggestions that there is a proportionately increased degree of oxidation in the apoE Ϫ/Ϫ mice (31,32). The "antioxidant" properties of apoE may account for the apparently higher rate of accumulation of EO6 reactivity on hLDL in apoE Ϫ/Ϫ mice compared with the absence of this accumulation in LDL receptor-deficient mice.…”

Section: Discussionsupporting

confidence: 89%

Autoantibodies to OxLDL fail to alter the clearance of injected OxLDL in apolipoprotein E-deficient mice

Reardon

Miller

Blachowicz

et al. 2004

Journal of Lipid Research

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This study tests the hypothesis that autoantibodies to oxidation epitopes on oxidized LDL (OxLDL) promote the clearance of OxLDL from the plasma. Human LDL (hLDL) was injected into immune-competent apolipoprotein E-deficient (apoE ؊ / ؊ ) mice and immune-deficient apoE ؊ / ؊ /recombination-activating gene-deficient mice that lack mature T and B cells and thus antibodies. There was a progressive decrease in human apoB-100 in the plasma in all mice, but the rate of clearance was not greater in the immune-competent mice than in the immune-deficient mice. Interestingly, oxidized phospholipid (OxPL) epitopes as detected by the EO6 antibody on the hLDL increased over time, suggesting de novo oxidation of the LDL or transfer of OxPL to the particles. Because the native LDL was not extensively modified, we also examined the clearance of copper OxLDL. Although the extensively OxLDL was cleared faster than the native LDL, there was no difference in the rate of clearance as a function of immune status. There appeared to be some transfer of OxPL to the endogenous murine LDL. Together, these results suggest that oxidation-specific antibodies do not participate to any great extent in the clearance of OxLDL from plasma. However, it is possible that such antibodies may bind to oxidation epitopes and modulate lesion formation within the vessel

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Section: Discussionsupporting

confidence: 89%

Autoantibodies to OxLDL fail to alter the clearance of injected OxLDL in apolipoprotein E-deficient mice

Reardon

Miller

Blachowicz

et al. 2004

Journal of Lipid Research

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“…23 Hypercholesterolaemia in animal models, as well as in humans, was shown to be associated with increased oxidative stress, both in plasma and in aorta. 24,25 Thus, cellular oxidative stress in hypercholesterolaemic animals could participate in the regulation of the AT 1 -receptor.…”

Section: Discussionmentioning

confidence: 99%

“…27 In apolipoprotein E deficient (E 0 ) mice, spontaneous hypercholesterolaemia 28 and accelerated atherosclerosis 29 were observed in association with lipid peroxidation, which occurred in plasma, and was further enhanced in the arterial wall. 25,30,31 The presence of lipid peroxides and oxysterols was shown in the blood monocytes of E 0 mice and in macrophages isolated from the aortae of these mice (as well as from human carotid arteries). 6 In atherosclerotic E 0 mice, Ang II substantially accelerated the build-up of atherosclerotic lesions in association with the formation of cholesterol-loaded foam cells.…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress increases the expression of the angiotensin-II receptor type 1 in mouse peritoneal macrophages

Keidar

Heinrich

Kaplan

et al. 2002

J Renin Angiotensin Aldosterone Syst

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Angiotensin II (Ang II) has been shown to accelerate atherogenesis, and the cellular Ang II type 1 (AT 1 ) -receptor mediates most of Ang II-induced proatherogenic effects. In this study we have examined the effect of macrophage oxidative stress on cellular AT 1 -receptor expression.Mouse peritoneal macrophages (MPM) from apolipoprotein-E deficient (E 0 ) mice at increasing ages (1-6 months) demonstrated an age-dependent increase in cellular lipid-peroxides (PD) content. In parallel, the AT 1 -receptor mRNA and protein levels both increased by up to 3.7-fold and 1.7-fold, respectively, in MPM from 6-month old mice compared with 1-month old mice. Vitamin E supplementation to E 0 mice significantly decreased the MPM PD content and macrophage AT 1 -receptor mRNA expression compared with placebo-treated mice. The role of oxidative stress in the cellular expression of AT 1 -receptors was further demonstrated by manipulation of macrophage glutathione content. Buthionine-sulfoximine, a glutathione synthesis inhibitor, increased MPM PD content and AT 1 -receptor mRNA expression, whereas L-2-oxothiazolidine-4-carboxylic acid, that contributes to glutathione synthesis, reduced macrophage PD and AT 1 -receptor mRNA expression. Incubation of MPM with oxidised low-density lipoproteins (LDL) led to a significant, dose-dependent and time-dependent increase in macrophage AT 1 -receptor mRNA and protein expression, compared with control cells. In contrast, native LDL or acetylated LDL did not significantly affect macrophage AT 1 -receptor mRNA expression.In conclusion, our findings suggest that oxidative stress in macrophages induces AT 1 -receptor expression. This phenomenon can stimulate the interaction of Ang II with macrophages and hence accelerate macrophage foam cell formation and early atherogenesis.

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“…Th e presence of recombinant human ApoE ε2 in primary mixed neuronal-glial cell cultures partially protected against oxidative injury by reducing secondary glutamate excitotoxicity 23 . Furthermore, ApoE deficient mice are more prone to oxidative tissue damage after ischemia than mice with normal ApoE production 8 . Similarly, transgenic mice with the ApoE ε3/3 genotype have a better neurological outcome and survival rate after ischemic and oxidative stress than mice with the ApoE ε4/4 genotype 9,24 .…”

Section: Discussionmentioning

confidence: 99%

“…ApoE defi ciency has been shown to adversely aff ect outcome after transient cerebral ischemia and head trauma. Since oxidative stress contributes to these injuries, the ability of ApoE to reduce irreversible oxidative damage was studied 8,9 . Th e ApoE gene is a confi rmed genetic risk factor that infl uences both the risk and age at onset of Alzheimer's disease and Parkinson's disease 10 .…”

Section: Introductionmentioning

confidence: 99%

Is Apolipoprotein E ε2 Associated with Delayed Onset of Non-Lesional Temporal Lobe Epilepsy?

Sporiš

Bašić

Sertić

et al. 2017

acc

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SUMMARY -Th e aim of the study was to evaluate the possible association between Apo E polymorphisms and age at seizure onset in patients with non-lesional temporal lobe epilepsy. Eighty patients with non-lesional temporal lobe epilepsy with or without bilateral tonic-clonic propagation were analyzed. Age at seizure onset was defi ned as age at the fi rst unequivocal seizure (excluding febrile convulsions). ApoE alleles were determined by a procedure where genome DNA was amplifi ed by chain reaction along with polymerase, using the LightCycler kit (Roche) for ApoE mutations on codons 112 and 158. Th ere was a statistically signifi cant diff erence between the groups of patients with ApoE ε2/3 and ε3/4 genotypes (p=0.03), but not between patients with ApoE ε2/3 and ε3/3, and those with ApoE ε3/4 and ε3/3. In conclusion, the results of our study suggested positive association of a specifi c ApoE genotype and onset of non-lesional temporal lobe epilepsy.

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Increased Plasma and Lipoprotein Lipid Peroxidation in apo E-Deficient Mice

Cited by 168 publications

References 0 publications

Autoantibodies to OxLDL fail to alter the clearance of injected OxLDL in apolipoprotein E-deficient mice

Autoantibodies to OxLDL fail to alter the clearance of injected OxLDL in apolipoprotein E-deficient mice

Oxidative stress increases the expression of the angiotensin-II receptor type 1 in mouse peritoneal macrophages

Is Apolipoprotein E ε2 Associated with Delayed Onset of Non-Lesional Temporal Lobe Epilepsy?

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