Search results for "Apoe"

showing 10 items of 43 documents

CD36 gene polymorphism is associated with Alzheimer's disease.

2017

IF 3.112; International audience; CD36 gene encodes a membrane glycoprotein (type B scavenger receptor) present on the surface of many types of cells and having multiple cellular functions ranging from angiogenesis to gustatory perception of fatty acids. Using a case control genetic association approach we have analyzed selected single nucleotide polymorphisms (SNP's) in a total of 859 patients with Alzheimer's disease (AD) and controls and have identified the allele A in rs3211892 polymorphism of CD36 gene as significantly increasing the risk of AD. Additionally we have investigated, in the same sample of control subjects and patients, SNP's in ApoE gene and confirmed that the previously i…

0301 basic medicineApolipoprotein EMESH : Oxidative StressCD36 AntigensMaleMESH : Polymorphism GeneticCD36MESH : AgedMESH : Alzheimer DiseaseMESH : GenotypeBiochemistryGeneMESH: Genotype0302 clinical medicineMESH: CholesterolMESH : FemaleMESH : CholesterolGeneticsMESH: AgedMESH: Oxidative StressbiologyMESH: Polymorphism Single NucleotideMESH : Polymorphism Single NucleotideMESH: Genetic Predisposition to DiseaseGeneral Medicine3. Good healthMESH : Antigens CD36CholesterolInterleukin 18FemaleApoEGenotypeMESH : MaleSingle-nucleotide polymorphismPolymorphism Single NucleotideMMSEAssociation03 medical and health sciencesAlzheimer DiseaseMESH: Polymorphism GeneticSNPHumansGenetic Predisposition to Disease[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAllelePolymorphism[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyGenetic associationAgedPolymorphism GeneticMESH: HumansMESH: Antigens CD36MESH : HumansMESH: MaleOxidative Stress030104 developmental biologybiology.proteinMESH : Genetic Predisposition to DiseaseGene polymorphismCD36MESH: Female030217 neurology & neurosurgeryMESH: Alzheimer Disease
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Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

2018

Objective— Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N -acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-α (peroxisome proliferator-activated receptors α) and the orphan receptor GPR55. Palmitoylethanolamide exerts potent anti-inflammatory actions but its physiological role and promise as a therapeutic agent in chronic arterial inflammation, such as atherosclerosis remain unexplored. Approach and Results— First, the polarization of mouse primary macrophages towards a proinflammatory phenotype was found to reduce N -acyl phosphatidylethanolamine phospholipase D expression …

0301 basic medicineCannabinoid receptorTime FactorsMice Knockout ApoECHOLESTEROL TRANSPORTAnti-Inflammatory AgentsPhospholipaseProto-Oncogene Maschemistry.chemical_compoundCannabinoid receptor type 2Receptors CannabinoidAortachemistry.chemical_classificationMARROW-DERIVED CELLSAPOPTOTIC CELL ACCUMULATIONPlaque AtheroscleroticCell biologymacrophagesDENSITY-LIPOPROTEIN RECEPTORPhenotypeREDUCES INFLAMMATIONCB2 RECEPTOREthanolaminesFemaleCardiology and Cardiovascular MedicineSCAVENGER RECEPTORAortic DiseasesPalmitic Acidsta3111fatty acidsCell Line03 medical and health sciencesMediatorPhagocytosisPhospholipase DAnimalsHumansScavenger receptorCANNABINOID RECEPTORPhosphatidylethanolaminePalmitoylethanolamidec-Mer Tyrosine KinaseFatty acidcholesterolta3121AmidesRatsMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryinflammationRECEPTOR CLASS-BatherosclerosisCONTACT ALLERGIC DERMATITISArteriosclerosis Thrombosis and Vascular Biology
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GRIP1 Binds to ApoER2 and EphrinB2 to Induce Activity-Dependent AMPA Receptor Insertion at the Synapse

2017

Summary Regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor trafficking in response to neuronal activity is critical for synaptic function and plasticity. Here, we show that neuronal activity induces the binding of ephrinB2 and ApoER2 receptors at the postsynapse to regulate de novo insertion of AMPA receptors. Mechanistically, the multi-PDZ adaptor glutamate-receptor-interacting protein 1 (GRIP1) binds ApoER2 and bridges a complex including ApoER2, ephrinB2, and AMPA receptors. Phosphorylation of ephrinB2 in a serine residue (Ser-9) is essential for the stability of such a complex. In vivo, a mutation on ephrinB2 Ser-9 in mice results in a complete disruption…

0301 basic medicineLong-Term PotentiationPrimary Cell CultureEphrin-B2Mice TransgenicNerve Tissue ProteinsephrinBAMPA receptorGRIP1BiologyHippocampusArticleApoER2General Biochemistry Genetics and Molecular BiologyPostsynapseMice03 medical and health sciences0302 clinical medicineddc:570SerineAnimalsReceptors AMPAPhosphorylationAMPA receptorsLong-term depressionlcsh:QH301-705.5LDL-Receptor Related ProteinsAdaptor Proteins Signal TransducingNeuronssynaptic plasticitySynaptic scalingLong-term potentiationCell biologyProtein Transport030104 developmental biologyGene Expression Regulationlcsh:Biology (General)nervous systemSynapsesSilent synapseSynaptic plasticityLTP030217 neurology & neurosurgeryIon channel linked receptorsProtein BindingSignal TransductionCell Reports
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CAMKIIγ suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis

2017

Atherosclerosis is the underlying etiology of cardiovascular disease, the leading cause of death worldwide. Atherosclerosis is a heterogeneous disease in which only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death. A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates these acute events. Here, we show that Ca2+/calmodulin-dependent protein kinase gamma (CaMKII gamma) in macrophages plays a major role in the development of necrotic, thin-capped plaques. Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation of CaMKII. We…

0301 basic medicineMalePathologymedicine.medical_specialtyPhagocytosisGene ExpressionInflammationApoptosisMice TransgenicBiologyPHAGOCYTOSISLIPID MEDIATORS03 medical and health sciencesNecrosisENDOPLASMIC-RETICULUM STRESSINFLAMMATIONCa2+/calmodulin-dependent protein kinaseC/EBP HOMOLOGOUS PROTEINmedicineMacrophageAnimalsHumansKINASE-IILiver X receptorEfferocytosisCells CulturedLiver X ReceptorsAPOE-DEFICIENT MICEc-Mer Tyrosine KinaseATF6MacrophagesAPOPTOTIC CELL ACCUMULATIONGeneral MedicineMERTKAtherosclerosisPlaque AtheroscleroticActivating Transcription Factor 6Enzyme ActivationMice Inbred C57BL030104 developmental biologyRESOLUTIONmedicine.symptomCalcium-Calmodulin-Dependent Protein Kinase Type 2LIVER-X-RECEPTORResearch ArticleSignal TransductionJournal of Clinical Investigation
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Functional role of endothelial CXCL16/CXCR6-platelet-leucocyte axis in angiotensin II-associated metabolic disorders.

2018

Aims Angiotensin-II (Ang-II) is the main effector peptide of the renin-angiotensin system (RAS) and promotes leucocyte adhesion to the stimulated endothelium. Because RAS activation and Ang-II signalling are implicated in metabolic syndrome (MS) and abdominal aortic aneurysm (AAA), we investigated the effect of Ang-II on CXCL16 arterial expression, the underlying mechanisms, and the functional role of the CXCL16/CXCR6 axis in these cardiometabolic disorders. Methods and results Results from in vitro chamber assays revealed that CXCL16 neutralization significantly inhibited mononuclear leucocyte adhesion to arterial but not to venous endothelial cells. Flow cytometry and immunofluorescence s…

0301 basic medicineMaleRHOAPhysiologyMice Knockout ApoE030204 cardiovascular system & hematology0302 clinical medicineLeukocytesReceptorCells CulturedMetabolic SyndromebiologyChemistryAngiotensin IIMiddle AgedAortic AneurysmVascular endothelial growth factor ALosartanmedicine.anatomical_structurecardiovascular systemFemaleCardiology and Cardiovascular Medicinemedicine.drugSignal TransductionAdultBlood Plateletsmedicine.medical_specialtyEndothelium03 medical and health sciencesPhysiology (medical)Internal medicinemedicineCell AdhesionAnimalsHumansPlatelet activationReceptors CXCR6Angiotensin II receptor type 1Endothelial CellsChemokine CXCL16Platelet ActivationAngiotensin IICoculture TechniquesMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyCase-Control Studiesbiology.proteinAngiotensin II Type 1 Receptor BlockersCardiovascular research
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Changes in CDKN2A/2B expression associate with T-cell phenotype modulation in atherosclerosis and type 2 diabetes mellitus.

2018

Previous studies indicate a role of CDKN2A/2B/2BAS genes in atherosclerosis and type 2 diabetes mellitus (T2DM). Progression of these diseases is accompanied by T-cell imbalance and chronic inflammation. Our main objective was to investigate a potential association between CDKN2A/2B/2BAS gene expression and T cell phenotype in T2DM and coronary artery disease (CAD) in humans, and to explore the therapeutic potential of these genes to restore immune cell homeostasis and disease progression. Reduced mRNA levels of CDKN2A (p16Ink4a), CDKN2B (p15Ink4b), and CDKN2BAS were observed in human T2DM and T2DM-CAD subjects compared with controls. Protein levels of p16Ink4a and p15Ink4b were also dimini…

0301 basic medicineMalemedicine.medical_specialtyendocrine system diseasesMice Knockout ApoECD3T cellCD14Inflammation03 medical and health sciencesMice0302 clinical medicinePhysiology (medical)Internal medicineNeointimamedicineAnimalsHumansIL-2 receptorInterleukin-7 receptorneoplasmsbiologybusiness.industryGenes p16Biochemistry (medical)CDKN2BASPublic Health Environmental and Occupational HealthType 2 Diabetes MellitusGeneral MedicineAtherosclerosis030104 developmental biologyEndocrinologymedicine.anatomical_structureDiabetes Mellitus Type 2030220 oncology & carcinogenesisbiology.proteinLeukocytes Mononuclearmedicine.symptombusinessTranslational research : the journal of laboratory and clinical medicine
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Oxidative signature of cerebrospinal fluid from mild cognitive impairment and Alzheimer disease patients

2015

Abstract Background Several studies suggest that pathological changes in Alzheimer’s disease (AD) brain begin around 10–20 years before the onset of cognitive impairment. Biomarkers that can support early diagnosis and predict development of dementia would, therefore, be crucial for patient care and evaluation of drug efficacy. Although cerebrospinal fluid (CSF) levels of Aβ42, tau, and p-tau are well-established diagnostic biomarkers of AD, there is an urgent need to identify additional molecular alterations of neuronal function that can be evaluated at the systemic level. Objectives This study was focused on the analysis of oxidative stress-related modifications of the CSF proteome, from …

0301 basic medicineOncologyPathologyDiseasephysiology (medical)medicine.disease_causeProtein oxidationtau proteins0302 clinical medicineCerebrospinal fluidmiddle aged80 and overoxidative stresshumansAged 80 and overamyloid beta-peptidesredox proteomicsagedfemale030220 oncology & carcinogenesisBiomarker (medicine)Alzheimer's diseaseAlzheimer diseaseAPOEmedicine.medical_specialtyoxidation-reductionproteomeCSFmolecular sequence data03 medical and health sciencesmalecognitive dysfunctionInternal medicinemental disordersmedicineDementiabiochemistryprotein oxidationbusiness.industrypeptide fragmentscase-control studiesCase-control studybiomarkersmedicine.diseaseAPOE; biomarkers; CSF; extracellular chaperones; protein oxidation; redox proteomics; aged; aged 80 and over; Alzheimer disease; amino acid sequence; amyloid beta-peptides; apolipoproteins E; biomarkers; case-control studies; cognitive dysfunction; female; humans; male; middle aged; molecular sequence data; oxidation-reduction; oxidative stress; peptide fragments; proteome; tau proteins; biochemistry; physiology (medical)extracellular chaperonesamino acid sequence030104 developmental biologybusinessOxidative stressapolipoproteins E
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The Vitamin D Receptor Regulates Glycerolipid and Phospholipid Metabolism in Human Hepatocytes.

2020

The vitamin D receptor (VDR) must be relevant to liver lipid metabolism because VDR deficient mice are protected from hepatosteatosis. Therefore, our objective was to define the role of VDR on the overall lipid metabolism in human hepatocytes. We developed an adenoviral vector for human VDR and performed transcriptomic and metabolomic analyses of cultured human hepatocytes upon VDR activation by vitamin D (VitD). Twenty percent of the VDR responsive genes were related to lipid metabolism, including MOGAT1, LPGAT1, AGPAT2, and DGAT1 (glycerolipid metabolism)

0301 basic medicinemusculoskeletal diseasesmedicine.medical_specialtyVitaminesLithocholic acidMice Knockout ApoECèl·luleslcsh:QR1-502Phospholipidvitamin DBiochemistryCalcitriol receptorlcsh:MicrobiologyArticle03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineBiomolèculesDownregulation and upregulationInternal medicinelipid metabolismmedicinepolycyclic compoundsAnimalsHumansvitamin D receptorMolecular BiologyPhospholipidsTriglyceridesPhosphatidylethanolaminedigestive oral and skin physiologyhuman hepatocytesLipid metabolismMetabolismHep G2 Cells030104 developmental biologyEndocrinologychemistryGene Expression Regulation030220 oncology & carcinogenesisHepatocytesReceptors Calcitriollipids (amino acids peptides and proteins)IntracellularBiomolecules
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Acute Myocardial Infarction and Proinflammatory Gene Variants

2007

We identified four genetic risk sets for acute myocardial infarction (AMI) from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF -308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE ε2/3/4; 316 patients and 461 healthy subjects, all Italian. Putative risk alleles are shown underlined. The sets were identified using grade-of-membership analysis. Membership scores in the sets are automatically generated for individuals. The ''low intrinsic risk'' set had alleles that downregulate inflammation and cholesterol synthesis (IL6, TNF, ILl0, HMGCR). ''AMI across a broad age range'' carried multiple pr…

AdultMaleApolipoprotein EAdolescentMyocardial InfarctionGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokinePathogenesischemistry.chemical_compoundApolipoproteins EHistory and Philosophy of SciencemedicineHumansGenetic Predisposition to DiseaseMyocardial infarctionAge of OnsetAlleleAllelesSerpinsAgedAged 80 and overbusiness.industryCholesterolGeneral NeuroscienceMiddle Agedmedicine.diseaseMiddle ageInterleukin 10CholesterolchemistryAMI Grade of Membership Genetic profile IL6 -174 G/C TNF -308 G/A IL10 -1082 G/A SERPINA3 -51 G/T IFNG +874 T/A HMGCR -911 C/A APOE ε2/3/4Acute DiseaseImmunologyCytokinesFemaleHydroxymethylglutaryl CoA Reductaseslipids (amino acids peptides and proteins)businessAnnals of the New York Academy of Sciences
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G×E Interaction Influences Trajectories of Hand Grip Strength.

2016

Age-related decline in grip strength predicts later life disability, frailty, lower well-being and cognitive change. While grip strength is heritable, genetic influence on change in grip strength has been relatively ignored, with non-shared environmental influence identified as the primary contributor in a single longitudinal study. The extent to which gene-environment interplay, particularly gene-environment interactions, contributes to grip trajectories has yet to be examined. We considered longitudinal grip strength measurements in seven twin studies of aging in the Interplay of Genes and Environment across Multiple Studies consortium. Growth curve parameters were estimated for same-sex …

AdultMaleLongitudinal studyAgingTwinsTwins Monozygotic/geneticsBiologyEnvironmentArticle03 medical and health sciencesGrip strength0302 clinical medicineApolipoproteins ECognitive changeHand strengthGeneticsHumans030212 general & internal medicineHand Strength/physiologyAging/psychologyLongitudinal StudiesGene–environment interactionGenetics (clinical)Ecology Evolution Behavior and SystematicsAgedAged 80 and overHand StrengthAge FactorsGrowth curve (biology)Twins MonozygoticMiddle AgedTwin studyGene-environment interactionkaksosetGrip strengthFemaleGene-Environment InteractionApolipoproteins E/genetics030217 neurology & neurosurgeryAPOEDemographyBehavior genetics
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