Search results for "Apolipoproteins E"

showing 10 items of 80 documents

Effect of rat plasma high density lipoprotein with or without apolipoprotein E on the cholesterol uptake and on the induction of the corticosteroid b…

1991

Abstract High density lipoprotein (HDL) has been shown to induce the cellular accumulation of cholesterol esters and the biosynthesis of 21-hydroxysteroids (corticosteroids) newborn rat adrenocortical cells cultivated in serum-free medium. In order to identify the component(s) of HDL responsible for these effects, we investigated the ability of rat HDL subfractions and HDL with or without apolipoprotein E to deliver cholesterol to cells and to stimulate the steroid biosynthetic pathways in adrenal cultured cells. The total cholesterol uptake from HDL 2 was greater than that observed with HDL rich in apolipoprotein E (HDL 1 and HDL c ). Furthermore, the increase of the ratio between 21-hydro…

Apolipoprotein Emedicine.medical_specialtyApolipoprotein Bmedicine.medical_treatmentBiologySteroidMicechemistry.chemical_compoundApolipoproteins EHigh-density lipoproteinBiosynthesisAdrenal Cortex HormonesCorticosteroneInternal medicinemedicineAnimalsMolecular BiologyCells CulturedCholesterolnutritional and metabolic diseasesCell BiologyRatsLipoproteins LDLCholesterolEndocrinologyAnimals NewbornchemistryAdrenal Cortexbiology.proteinlipids (amino acids peptides and proteins)Apolipoprotein C2Lipoproteins HDLBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Knock-down of the oxysterol receptor LXRα impairs cholesterol efflux in human primary macrophages: lack of compensation by LXRβ activation.

2012

Liver X Receptors (LXRs) α and β are oxysterol-activated nuclear receptors involved in the control of lipid metabolism and inflammation. Pharmacological activation of LXR is promising in the treatment of atherosclerosis since it can promote cholesterol efflux from macrophages and prevent foam cell formation. However, the development of LXR agonists has been limited by undesirable side-effects such as hepatic steatosis mediated by LXRα activation. Therefore, it has been proposed that targeting LXRα activators to extrahepatic tissues or using LXRβ-specific activators could be used as alternative strategies. It is not clear whether these molecules will retain the full atheroprotective potentia…

Apolipoprotein Emedicine.medical_specialtyBenzylaminesOxysterolHydrocarbons FluorinatedPrimary Cell CultureBiochemistryBenzoatesApolipoproteins EInternal medicinemedicineHumansRNA Small InterferingReceptorLiver X receptorCells CulturedFoam cellLiver X ReceptorsPharmacologySulfonamidesbiologyApolipoprotein A-IMacrophagesOrphan Nuclear ReceptorsLipoproteins HDL2Cell biologyEndocrinologyCholesterolABCG1Nuclear receptorABCA1Gene Knockdown Techniquesbiology.proteinlipids (amino acids peptides and proteins)Biochemical pharmacology
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Deficiency of glutathione peroxidase-1 accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.

2007

Background— We have recently demonstrated that activity of red blood cell glutathione peroxidase-1 is inversely associated with the risk of cardiovascular events in patients with coronary artery disease. The present study analyzed the effect of glutathione peroxidase-1 deficiency on atherogenesis in the apolipoprotein E-deficient mouse. Methods and Results— Female apolipoprotein E-deficient mice with and without glutathione peroxidase-1 deficiency were placed on a Western-type diet for another 6, 12, or 24 weeks. After 24 weeks on Western-type diet, double-knockout mice (GPx-1 −/− ApoE −/− ) developed significantly more atherosclerosis than control apolipoprotein E-deficient mice. Moreover…

Apolipoprotein Emedicine.medical_specialtyGPX1AntioxidantApolipoprotein Bmedicine.medical_treatmentLipoproteinsApoptosisBlood Pressuremedicine.disease_causeNitric OxideMitochondria HeartMonocyteschemistry.chemical_compoundMiceApolipoproteins EGlutathione Peroxidase GPX1SuperoxidesInternal medicinePeroxynitrous AcidmedicineAnimalsAortaCell Proliferationchemistry.chemical_classificationMice KnockoutReactive oxygen speciesGlutathione PeroxidaseMembranesbiologyGlutathione peroxidaseGlutathioneAtherosclerosisEndocrinologyPhenotypechemistryImmunologybiology.proteinDisease ProgressionFemaleCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidation-ReductionOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Reduced VLDL clearance in ApoeNpc1 mice is associated with increased Pcsk9 and Idol expression and decreased hepatic LDL-receptor levels

2010

Niemann-Pick type C1 (NPC1) promotes the transport of LDL receptor (LDL-R)-derived cholesterol from late endosomes/lysosomes to other cellular compartments. NPC1-deficient cells showed impaired regulation of liver_X receptor (LXR) and sterol regulatory element-binding protein (SREBP) target genes. We observed that Apoe(-/-)Npc1(-/-) mice displayed a marked increase in total plasma cholesterol mainly due to increased VLDL, reflecting decreased clearance. Although nuclear SREBP-2 and Ldlr mRNA levels were increased in Apoe(-/-)Npc1(-/-) liver, LDL-R protein levels were decreased in association with marked induction of proprotein convertase subtilisin/kexin type 9 (Pcsk9) and inducible degrade…

Apolipoprotein EreceptorCholesterol VLDLLDL/metabolismMacrophages Peritoneal/cytologyBiochemistryMiceEndocrinologyhemic and lymphatic diseasesReceptorsOrphan Nuclear Receptors/geneticspolycyclic compoundsnuclear receptorCells CulturedResearch ArticlesLiver X ReceptorsMice KnockoutCulturedSterol Regulatory Element Binding Protein 2/geneticslipoproteinSerine EndopeptidasesIntracellular Signaling Peptides and ProteinsLamin Type AOrphan Nuclear ReceptorsTriglycerides/bloodCholesterolLiverProteins/geneticsKexinlipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9Sterol Regulatory Element Binding Protein 1Niemann-Pick diseaseSterol Regulatory Element Binding Protein 2medicine.medical_specialtyCellsKnockoutUbiquitin-Protein LigasesReceptors LDL/metabolismSerine Endopeptidases/geneticsQD415-436BiologyCholesterol/blooddigestive systemApolipoproteins ELiver/physiologySterol Regulatory Element Binding Protein 1/geneticsNiemann-Pick C1 ProteinInternal medicinemedicineAnimalsPeritoneal/cytologyCholesterol VLDL/metabolismUbiquitin-Protein Ligases/geneticsLiver X receptorTriglyceridesMacrophagesPCSK9Proteinsnutritional and metabolic diseasesVLDL/metabolismLamin Type A/metabolismCell BiologySterol regulatory element-binding proteinEndocrinologyReceptors LDLLDL receptorMacrophages PeritonealSterol regulatory element-binding protein 2atherosclerosisApolipoproteins E/geneticsLipoproteinJournal of Lipid Research
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Inflammation, genes and zinc in Alzheimer's disease.

2007

Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease which in Western society mainly accounts for clinical dementia. AD has been linked to inflammation and metal biological pathway. Neuro-pathological hallmarks are senile plaques, resulting from the accumulation of several proteins and an inflammatory reaction around deposits of amyloid, a fibrillar protein, Abeta, product of cleavage of a much larger protein, the beta-amyloid precursor protein (APP) and neurofibrillary tangles. Amyloid deposition, due to the accumulation of Abeta peptide, is the main pathogenetic mechanism. Inflammation clearly occurs in pathologically vulnerable regions of AD and several i…

BACE1-ASInflammationBiologyModels BiologicalBiological pathwayApolipoproteins EAlzheimer Diseasemental disordersmedicineAnimalsHumansSenile plaquesInflammation genes zinc Alzheimer's diseaseSettore MED/04 - Patologia GeneraleInflammationAmyloid beta-PeptidesGeneral NeuroscienceP3 peptidemedicine.diseasePhenotypeBiochemistry of Alzheimer's diseaseZincCholesterolImmunologyCytokinesNeurology (clinical)Alzheimer's diseasemedicine.symptomBrain research reviews
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Impact of Glutathione Peroxidase-1 Deficiency on Macrophage Foam Cell Formation and Proliferation: Implications for Atherogenesis

2013

Clinical and experimental evidence suggests a protective role for the antioxidant enzyme glutathione peroxidase-1 (GPx-1) in the atherogenic process. GPx-1 deficiency accelerates atherosclerosis and increases lesion cellularity in ApoE(-/-) mice. However, the distribution of GPx-1 within the atherosclerotic lesion as well as the mechanisms leading to increased macrophage numbers in lesions is still unknown. Accordingly, the aims of the present study were (1) to analyze which cells express GPx-1 within atherosclerotic lesions and (2) to determine whether a lack of GPx-1 affects macrophage foam cell formation and cellular proliferation. Both in situ-hybridization and immunohistochemistry of l…

CD36 AntigensMAPK/ERK pathwayMouseMitogen-Activated Protein Kinase 3lcsh:MedicineGene ExpressionSignal transductionCardiovascularMiceMolecular cell biologyGlutathione Peroxidase GPX1lcsh:ScienceIn Situ HybridizationFoam cellMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryReverse Transcriptase Polymerase Chain ReactionKinaseSignaling cascadesScavenger Receptors Class AAnimal ModelsImmunohistochemistryLipoproteins LDLMedicineFemaleSignal transductionResearch ArticleMacrophage colony-stimulating factorMAPK signaling cascadesBlotting WesternBiologyCell GrowthModel OrganismsApolipoproteins EVascular BiologyAnimalsHumansProtein kinase ABiologyCell ProliferationGlutathione PeroxidaseMacrophage Colony-Stimulating Factorlcsh:RAtherosclerosisMolecular biologyMacrophages Peritoneallcsh:QMacrophage proliferationFoam CellsPLoS ONE
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Development of Abdominal Aortic Aneurysm Is Decreased in Mice with Plasma Phospholipid Transfer Protein Deficiency

2013

International audience; Plasma phospholipid transfer protein (PLTP) increases the circulating levels of proatherogenic lipoproteins, accelerates blood coagulation, and modulates inflammation. The role of PLTP in the development of abdominal aortic aneurysm (AAA) was investigated by using either a combination of mechanical and elastase injury at one site of mouse aorta (elastase model) or continuous infusion of angiotensin II in hyperlipidemic ApoE-knockout mice (Ang II model). With the elastase model, complete PLTP deficiency was associated with a significantly lower incidence and a lesser degree of AAA expansion. With the Ang II model, findings were consistent with those in the elastase mo…

CD4-Positive T-LymphocytesMalemedicine.medical_specialty[SDV]Life Sciences [q-bio]Inflammation030204 cardiovascular system & hematologyBiologyPathology and Forensic MedicineMice03 medical and health sciencesAortic aneurysmApolipoproteins E0302 clinical medicinemedicine.arteryPhospholipid transfer proteinInternal medicinemedicineAnimalsPhospholipid Transfer ProteinsPancreatic elastaseAorta030304 developmental biologyInflammationMice Knockout0303 health sciencesAortaPancreatic ElastaseAngiotensin IIMacrophagesElastasemedicine.diseaseAngiotensin IIElastinMice Inbred C57BL[SDV] Life Sciences [q-bio]EndocrinologyLiverImmunologybiology.proteincardiovascular systemCytokinesmedicine.symptomElastinAortic Aneurysm Abdominal
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Anti-angiogenic drug loaded liposomes: Nanotherapy for early atherosclerotic lesions in mice.

2018

Este artículo se encuentra disponible en la página web de la revista en la siguiente URL: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0190540 También participan en la elaboración de este artículo científico: Aracely Calatayud-Pascual, Alicia López-Castellano, Elena P. Albelda, Enrique García-España, Luis Martí-Bonmatí, Juan C. Frias y M. Teresa Albelda. Fumagillin-loaded liposomes were injected into ApoE-KO mice. The animals were divided into several groups to test the efficacy of this anti-angiogenic drug for early treatment of atherosclerotic lesions. Statistical analysis of the lesions revealed a decrease in the lesion size after 5 weeks of treatment.

Fluorescence-lifetime imaging microscopyPathologylcsh:MedicineAngiogenesis Inhibitors02 engineering and technology030204 cardiovascular system & hematologyVascular MedicineBiochemistryArteriosclerosis - Chemotherapy.Diagnostic RadiologyAteroesclerosis - Farmacoterapia.MiceWhite Blood Cells0302 clinical medicineAnimal CellsArteriosclerosis - Farmacoterapia.Medicine and Health SciencesArteries - Diseases - Treatment.Nanotechnologylcsh:ScienceAortaPhospholipidsmedia_commonMice KnockoutLiposomeDrug CarriersMultidisciplinarymedicine.diagnostic_testRadiology and Imaging021001 nanoscience & nanotechnologyMagnetic Resonance ImagingLipidsFatty Acids UnsaturatedEngineering and Technologymedicine.symptomCellular Structures and OrganellesCellular TypesAnatomy0210 nano-technologySesquiterpenesResearch ArticleDrugmedicine.medical_specialtyImaging Techniquesmedia_common.quotation_subjectImmune CellsImmunologyLiposomes.Research and Analysis MethodsLiposomas.Lesion03 medical and health sciencesText miningApolipoproteins ECyclohexanesDiagnostic Medicinemedicine.arteryFluorescence ImagingmedicineAnimalsArterias - Enfermedades - Tratamiento.VesiclesAortaBlood Cellsbusiness.industryMacrophageslcsh:RAnti angiogenicBiology and Life SciencesMagnetic resonance imagingCell BiologyAtherosclerosisFumagillin - Therapeutic use.Atherosclerosis - Chemotherapy.Disease Models AnimalFumagilina - Uso terapéutico.LiposomesCardiovascular AnatomyNanoparticlesBlood Vesselslcsh:QbusinessPloS one
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T Cell-Specific Overexpression of TGFß1 Fails to Influence Atherosclerosis in ApoE-Deficient Mice

2013

Clinical data have indicated a negative correlation between plasma TGFß1 concentrations and the extent of atherosclerosis and have thus led to the hypothesis that the pleiotropic cytokine may have anti-atherogenic properties. T-cells are currently discussed to significantly participate in atherogenesis, but the precise role of adaptive immunity in atherogenesis remains to be elucidated. TGFß1 is known to strongly modulate the function of T-cells, however, inhibition of TGFß1 signalling in T-cells of atherosclerosis-prone knock-out mice failed to unequivocally clarify the role of the cytokine for the development of atherosclerosis. In the present study, we thus tried to specify the role of T…

Genetically modified mouseApolipoprotein ELipoproteinsT-LymphocytesScienceCD3medicine.medical_treatmentT cellTransgeneMutantGene ExpressionMice TransgenicBiologyTransforming Growth Factor beta1MiceApolipoproteins EmedicineAnimalsHumansMultidisciplinaryQRAtherosclerosisAcquired immune systemCytokinemedicine.anatomical_structureImmunologyDisease Progressionbiology.proteinMedicineFemaleResearch ArticlePLoS ONE
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Overexpression of TGF-ß1 in macrophages reduces and stabilizes atherosclerotic plaques in ApoE-deficient mice.

2011

Although macrophages represent the hallmark of both human and murine atherosclerotic lesions and have been shown to express TGF-ß1 (transforming growth factor β1) and its receptors, it has so far not been experimentally addressed whether the pleiotropic cytokine TGF-ß1 may influence atherogenesis by a macrophage specific mechanism. We developed transgenic mice with macrophage specific TGF-ß1 overexpression, crossed the transgenics to the atherosclerotic ApoE (apolipoprotein E) knock-out strain and quantitatively analyzed both atherosclerotic lesion development and composition of the resulting double mutants. Compared with control ApoE(-/-) mice, animals with macrophage specific TGF-ß1 overe…

Genetically modified mouseApolipoprotein Emedicine.medical_specialtyPathologyHistologyMouseSciencemedicine.medical_treatmentImmune CellsImmunologyAntigen-Presenting CellsMice TransgenicBiologyCardiovascularLesionTransforming Growth Factor beta1MiceApolipoproteins EModel OrganismsVascular BiologyInternal medicinemedicineGeneticsMacrophageAnimalsReceptorBiologyMice KnockoutMultidisciplinaryMacrophagesQRAnimal ModelsAtherosclerosisImmunohistochemistryPlaque AtheroscleroticCytokineEndocrinologyImmunohistochemistryMedicineFemalemedicine.symptomGene FunctionTransforming growth factorResearch ArticlePloS one
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