Search results for "apolipoproteins E"

showing 10 items of 80 documents

Deficient p27 Phosphorylation at Serine 10 Increases Macrophage Foam Cell Formation and Aggravates Atherosclerosis Through a Proliferation-Independen…

2011

OBJECTIVE: Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide insight into both questions by investigating the role in atherosclerosis of p27 phosphorylation at serine 10 (p27-phospho-Ser10), a major posttranslational modification of this protein. METHODS AND RESULTS: Immunoblotting studies revealed a marked reduction in p27-phospho-Ser10 in atheroscleroti…

Malerho GTP-Binding ProteinsRHOAMoesinMiceApolipoproteins ERadixinSerinemedicineAnimalsHumansProtein phosphorylationPhosphorylationProtein kinase ACell ProliferationFoam cellMice Knockoutrho-Associated KinasesbiologyArteriesAtherosclerosismedicine.diseaseCell biologyMice Inbred C57BLDisease Models AnimalAtheromaCase-Control StudiesImmunologyDisease Progressionbiology.proteinPhosphorylationFemalerhoA GTP-Binding ProteinCardiology and Cardiovascular MedicineCyclin-Dependent Kinase Inhibitor p27Foam CellsSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Apolipoprotein E genotype does not influence the progression of multiple sclerosis

2003

OBJECTIVE: To investigate the association between apolipoprotein E (APOE) polymorphisms and the progression of MS. METHODS: We investigated 428 subjects affected by clinically defined MS, with a disease duration of at least three years. We collected data concerning the age at onset of MS, clinical type, disease duration and disability according to the expanded disability status scale (EDSS). We also calculated the progression index (PI) to evaluate disease progression. APOE genotyping and the -491 A/T polymorphism of the APOE promoter were determined. RESULTS: No association was observed between the APOE epsilon4 allele and clinical characteristics of our study population. We also investiga…

OncologyApolipoprotein EAdultMalemedicine.medical_specialtyMultiple SclerosisGenotypeAdolescentOdds Ratio; Polymorphism Genetic; Chi-Square Distribution; Humans; Disease Progression; Apolipoproteins E; Genotype; Multiple Sclerosis; Adult; Confidence Intervals; Adolescent; Statistics Nonparametric; Female; MalePopulationAPOE polymorphismBiologyStatistics NonparametricApolipoproteins EGeneticPolymorphism (computer science)Internal medicineGenotypeMultiple SclerosimedicineOdds RatioConfidence IntervalsHumansNonparametricPolymorphismeducationGenotypingAPOE promotereducation.field_of_studyExpanded Disability Status ScalePolymorphism GeneticChi-Square DistributionMS progressionStatisticsOdds ratioNeurologyImmunologyDisease ProgressionPopulation studylipids (amino acids peptides and proteins)FemaleSettore MED/26 - NeurologiaNeurology (clinical)Confidence IntervalHuman
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Genetic diagnosis of familial hypercholesterolemia in a South European outbreed population: influence of low-density lipoprotein (LDL) receptor gene …

2001

The aims of this study were to examine the presence of mutations in the low-density lipoprotein receptor gene among subjects clinically diagnosed with familial hypercholesterolemia and to analyze whether the molecular diagnosis helps to predict the response to simvastatin treatment in our familial hypercholesterolemia population. Fifty-five probands and 128 related subjects with familial hypercholesterolemia were studied. Genetic diagnosis was carried out following a three-step protocol based on Southern blot and PCR-single strand conformational polymorphism analysis. A randomized clinical trial with simvastatin was conducted in 42 genetically diagnosed subjects with familial hypercholester…

ProbandAdultMalemedicine.medical_specialtySimvastatinEndocrinology Diabetes and MetabolismClinical BiochemistryPopulationFamilial hypercholesterolemiaBiologyBiochemistryHyperlipoproteinemia Type IIchemistry.chemical_compoundEndocrinologyHigh-density lipoproteinApolipoproteins EInternal medicinemedicineHumanseducationAgedApolipoproteins Beducation.field_of_studyCholesterolBiochemistry (medical)Cholesterol HDLnutritional and metabolic diseasesCholesterol LDLMiddle Agedmedicine.diseaseEndocrinologychemistryReceptors LDLSimvastatinLow-density lipoproteinMutationlipids (amino acids peptides and proteins)FemaleHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteinmedicine.drugThe Journal of clinical endocrinology and metabolism
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Single tube optimisation of APOE genotyping based on melting curve analysis

2008

Objectives: To develop and validate a single-tube protocol for APOE genotyping using fluorescent probes. Design and methods: We have designed and validated a hybrid, single-tube, SimpleProbe/FRET probe protocol that takes advantage of the different probe wavelength emissions. Results: Our method offers high quality outcomes, minimum interferences between probe signals and is 100% concordant with the reference protocol. Conclusions: This method is cheaper, faster and more reliable and versatile than other alternatives proposed. © 2008 Elsevier Inc. All rights reserved.

Protocol (science)GenotypeComputer scienceClinical BiochemistryNanotechnologyGeneral MedicinePolymerase Chain ReactionMelting curve analysisSingle tubeApolipoproteins EValidation studiesCardiovascular DiseasesHumansThermodynamicsGenotypingAlgorithmAnalysisDNA PrimersClinical Biochemistry
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Genetic risk factors and candidate biomarkers for Alzheimer s disease

2009

Alzheimer's disease is a multifactorial and progressive neurodegenerative disease, extremely diffused and with an increasing prevalence worldwide. There is an urgent need for biomarkers to diagnose AD early in its course. Furthermore, accurate biomarkers would be able to determine the clinical efficacy of novel neuroprotective strategies. Although the heritability of late-onset AD is high, our knowledge of the underlying putative susceptibility genes remains incomplete and the only unequivocally established late-onset AD gene is APOE. Nevertheless a number of susceptibility loci seems to influence the pathogenesis of AD, and variations in numerous genes have been considered to be important …

Settore MED/04 - Patologia GeneraleApolipoprotein EAmyloid beta-PeptidesGeneral Immunology and MicrobiologyBiomarkers Alzheimer geneticbusiness.industryBrain dysfunctiontau ProteinsSusceptibility geneDiseaseBioinformaticsNeuroprotectionGeneral Biochemistry Genetics and Molecular BiologyPathogenesisApolipoproteins EAlzheimer DiseaseRisk FactorsSusceptibility locusHumansMedicineGenetic riskbusinessBiomarkersFrontiers in Bioscience
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Impact of estrogens on atherosclerosis and bone in the apolipoprotein E-deficient mouse model.

2014

Objective The common inflammatory pathophysiology has nourished the hypothesis of a relationship between osteoporosis and cardiovascular disease. Estrogens are key agents in the modulation of both processes. We investigated whether induction of atherosclerosis affects bone and whether estrogens modulate both processes. Methods Female apolipoprotein E-deficient mice (a well-established model of atherogenesis) were ovariectomized or falsely operated and fed either standard diet or high-fat diet (HFD). Six animals were included in each of the four groups. To clarify mechanisms, we treated preosteoblastic MC3T3-E1 cells with mouse serum. Results Physiological levels of estrogens in falsely oper…

medicine.medical_specialtyBone densityApolipoprotein BOvariectomyOsteoporosisDiet High-FatBone resorptionMiceApolipoproteins EBone DensityTrabecular PatternInternal medicinemedicineAnimalsHumansBone ResorptionBone mineralbiologybusiness.industryObstetrics and GynecologyEstrogensmedicine.diseaseAtherosclerosisDisease Models AnimalEndocrinologymedicine.anatomical_structureOvariectomized ratbiology.proteinOsteoporosisCortical boneFemalebusinessMenopause (New York, N.Y.)
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Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis.

2014

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing…

medicine.medical_specialtyVascular smooth musclePhysiologyCell Survivalmedicine.medical_treatmentMyocytes Smooth MuscleCX3C Chemokine Receptor 1InflammationMice TransgenicBiologyMuscle Smooth VascularInsulin resistanceApolipoproteins EPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayCells CulturedMice KnockoutChemokine CX3CL1Insulinmedicine.diseaseAtherosclerosisIRS2Mice Inbred C57BLAtheromaEndocrinologyDiabetes Mellitus Type 2cardiovascular systemReceptors Chemokinemedicine.symptomInsulin ResistanceCardiology and Cardiovascular MedicineSignal TransductionCardiovascular research
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Dietary cholate increases plasma levels of apolipoprotein B in mice by posttranscriptional mechanisms

2001

To induce atherogenesis in mice, a high fat (HF) diet is supplemented with cholic acid (CA), which increases apoB-containing particles and lower apoA-I-containing particles. HF diet without CA increases levels of both HDL and LDL, suggesting that CA may be responsible for the elevation of LDL and lowering of HDL. The mechanism of dietary CA-induced lowering of apoA-I-containing particles has recently been reported. In this study, we examined the mechanism of CA- and HF-induced elevation of apoB-containing lipoproteins in mice. Mice were fed the following four diets: control chow (C), high fat high cholesterol, (HF), control and 0.5% cholate (CA), and HF + CA. Dietary CA increased the plasma…

medicine.medical_specialtyVery low-density lipoproteinSettore MED/09 - Medicina InternaMouseApolipoprotein Bmedicine.medical_treatmentDown-RegulationCholic AcidLipoproteins VLDLBiochemistryDietary cholateMicechemistry.chemical_compoundApolipoproteins ERibonucleasesDownregulation and upregulationInternal medicinemedicineAnimalsVitamin ERNA MessengerRNA Processing Post-TranscriptionalReceptorApolipoproteins BbiologyChemistryVitamin ECholic acidnutritional and metabolic diseasesCell BiologyBlotting NorthernDietLipoproteins LDLMice Inbred C57BLCholesterolEndocrinologyLiverReceptors LDLLDL receptorbiology.proteinlipids (amino acids peptides and proteins)Gene expressionHepatic lipaseApolipoprotein BCholatesDietary fatThe International Journal of Biochemistry & Cell Biology
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Constitutive androstane receptor activation stimulates faecal bile acid excretion and reverse cholesterol transport in mice.

2010

The constitutive androstane receptor (CAR) is a nuclear receptor expressed in the liver and involved in xenobiotic metabolism. The aim of this study was to assess whether pharmacological CAR activation could affect neutral sterol and bile acid elimination under conditions of cholesterol overload.Wild type, Car-/-, ApoE-/-, and low-density lipoprotein receptor (Ldlr)-/- mice fed a western-type diet were treated with the CAR agonist TCPOBOP.CAR activation was associated with a decrease in faecal cholesterol output related to the repression of the Abcg5/g8 cholesterol transporters. In contrast, TCPOBOP treatment induced a marked increase (up to three fold, p0.01) in the elimination of faecal b…

medicine.medical_specialtymedicine.drug_classPyridinesLipoproteinsBiological Transport ActiveGene ExpressionReceptors Cytoplasmic and NuclearHyperlipidemiasBiologyCholesterol 7 alpha-hydroxylaseBile Acids and Saltschemistry.chemical_compoundFecesMiceApolipoproteins EInternal medicineConstitutive androstane receptormedicineAnimalsHomeostasisATP Binding Cassette Transporter Subfamily G Member 5Liver X receptorConstitutive Androstane ReceptorMice KnockoutHepatologyBile acidCholesterolReverse cholesterol transportATP Binding Cassette Transporter Subfamily G Member 8Cholesterol HDLAtherosclerosisSterolMice Inbred C57BLEndocrinologyCholesterolchemistryLiverReceptors LDLLDL receptorlipids (amino acids peptides and proteins)ATP-Binding Cassette TransportersJournal of hepatology
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Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis.

2005

Objective— Sedentary lifestyle is associated with increased cardiovascular events. The underlying molecular mechanisms are incompletely understood. Reactive oxygen species (ROS) contribute to endothelial dysfunction and atherosclerosis. An important source of vascular ROS is the NADPH oxidase. Methods and Results— C57BL6 mice were subjected to regular housing (physical inactivity) or voluntary training on running wheels (6 weeks). Inactivity increased vascular lipid peroxidation to 148±9% and upregulated superoxide release to 176±17% (L-012 chemiluminescence) and 188±29% (cytochrome C reduction assay), respectively. ROS production was predominantly increased in the endothelium and the medi…

rac1 GTP-Binding Proteinmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIArteriosclerosisNitric Oxide Synthase Type IIBiologymedicine.disease_causechemistry.chemical_compoundMiceApolipoproteins EInternal medicinePhysical Conditioning AnimalmedicineAnimalsNADH NADPH OxidoreductasesRNA MessengerEndothelial dysfunctionLife Stylechemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseSuperoxideNeuropeptidesNADPH Oxidase 1NADPH Oxidasesmedicine.diseasePhosphoproteinsMice Mutant Strainsrac GTP-Binding ProteinsMice Inbred C57BLVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologychemistryNOX1biology.proteinNADPH Oxidase 1Endothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressArteriosclerosis, thrombosis, and vascular biology
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