Search results for "LDL receptor"

showing 10 items of 62 documents

Germ-free housing conditions do not affect aortic root and aortic arch lesion size of late atherosclerotic low-density lipoprotein receptor-deficient…

2020

The microbiota has been linked to the development of atherosclerosis, but the functional impact of these resident bacteria on the lesion size and cellular composition of atherosclerotic plaques in the aorta has never been experimentally addressed with the germ-free low-density lipoprotein receptor-deficient (Ldlr(-/-)) mouse atherosclerosis model. Here, we report that 16 weeks of high-fat diet (HFD) feeding of hypercholesterolemicLdlr(-/-)mice at germ-free (GF) housing conditions did not impact relative aortic root plaque size, macrophage content, and necrotic core area. Likewise, we did not find changes in the relative aortic arch lesion size. However, late atherosclerotic GFLdlr(-/-)mice …

0301 basic medicineAortic archMalePathologyaortic rootAortic rootaortic archFunctional impactAorta ThoracicHYPERCHOLESTEROLEMIAMice0302 clinical medicineDeficient mouse610 Medicine & healthMice KnockoutBILE-ACIDSCellular compositionMicrobiotaCHOLESTEROLGUT MICROBIOTAGastroenterologyinflammatory markersHousing AnimalPlaque Atheroscleroticmacrophagessmooth muscle cellsInfectious Diseasesgerm-free030211 gastroenterology & hepatologyFemalelipids (amino acids peptides and proteins)SEXTRIMETHYLAMINEmedicine.symptomMicrobiology (medical)medicine.medical_specialty610 Medicine & healthBiologyMETABOLISMlesion sizeMicrobiologyLesion03 medical and health sciencesINFLAMMATIONmedicine.arterymedicineAnimalsGerm-Free LifeHumanslcsh:RC799-869AddendumMice Inbred C57BLDisease Models Animal030104 developmental biologyReceptors LDLlow-density lipoprotein receptor-deficient mouseageLDL receptorlcsh:Diseases of the digestive system. Gastroenterologyatherosclerosis
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Threshold Effects of Circulating Angiopoietin-Like 3 Levels on Plasma Lipoproteins.

2017

Abstract Context Angiopoietin-like 3 (ANGPTL3) deficiency in plasma due to loss-of-function gene mutations results in familial combined hypobetalipoproteinemia type 2 (FHBL2) in homozygotes. However, the lipid phenotype in heterozygotes is much milder and does not appear to relate directly to ANGPTL3 levels. Furthermore, the low-density lipoprotein (LDL) phenotype in carriers of ANGPTL3 mutations is unexplained. Objective To determine whether reduction below a critical threshold in plasma ANGPTL3 levels is a determinant of lipoprotein metabolism in FHBL2, and to determine whether proprotein convertase subtilisin kexin type 9 (PCSK9) is involved in determining low LDL levels in this conditio…

0301 basic medicineMaleApolipoprotein BEndocrinology Diabetes and MetabolismClinical BiochemistryBiochemistryLipoprotein particlePCSK9Cohort StudiesHypobetalipoproteinemiaschemistry.chemical_compoundEndocrinologyANGPTL3biologyChemistryMiddle AgedPedigreeLipoproteins LDLPhenotypeKexinlipids (amino acids peptides and proteins)FemaleANGPTL3; familial combined hypolipidemia; PCSK9Lipoproteins HDLAdultmedicine.medical_specialtyHeterozygoteBlotting Western03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseClinical Research ArticlesAgedAngiopoietin-Like Protein 3Apolipoproteins BCholesterolPCSK9Biochemistry (medical)medicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsLDL receptorMultivariate AnalysisMutationbiology.proteinLinear Modelsfamilial combined hypobetalipoproteinemiaHypobetalipoproteinemiaAngiopoietinsLipoprotein
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Simultaneous Inhibition of Peripheral CB1R and iNOS Mitigates Obesity-Related Dyslipidemia Through Distinct Mechanisms.

2020

Diabetic dyslipidemia, characterized by increased plasma triglycerides and decreased HDL cholesterol levels, is a major factor contributing to nonalcoholic steatohepatitis and cardiovascular risk in type 2 diabetes. Activation of the cannabinoid-1 receptor (CB1R) and activation of inducible nitric oxide synthase (iNOS) are associated with nonalcoholic steatohepatitis progression. Here, we tested whether dual-targeting inhibition of hepatic CB1R and iNOS improves diabetic dyslipidemia in mice with diet-induced obesity (DIO mice). DIO mice were treated for 14 days with (S)-MRI-1867, a peripherally restricted hybrid inhibitor of CB1R and iNOS. (R)-MRI-1867, the CB1R-inactive stereoisomer that …

0301 basic medicineMaleVery low-density lipoproteinEndocrinology Diabetes and MetabolismNitric Oxide Synthase Type II[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB][SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMice0302 clinical medicineReceptor Cannabinoid CB1[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]Receptor[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Cells Cultured[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismbiology[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Nitric oxide synthaseLiver[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyKexinlipids (amino acids peptides and proteins)medicine.medical_specialty[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]LipoproteinsImmunoblotting030209 endocrinology & metabolismReal-Time Polymerase Chain Reaction03 medical and health sciencesInternal medicineCommentariesInternal MedicinemedicineAnimalsObesity[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Dyslipidemiasbusiness.industry[SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT]PCSK9nutritional and metabolic diseases[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseLipid Metabolism[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMice Inbred C57BL030104 developmental biologyEndocrinologyGlucoseLDL receptorbiology.proteinHepatocytes[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologySteatosisbusinessDyslipidemia
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Bioactive triterpenes of protium heptaphyllum gum resin extract display cholesterol-lowering potential

2021

Hypercholesterolemia is one of the major causes of cardiovascular disease, the risk of which is further increased if other forms of dyslipidemia occur. Current therapeutic strategies include changes in lifestyle coupled with drug administration. Statins represent the most common therapeutic approach, but they may be insufficient due to the onset of resistance mechanisms and side effects. Consequently, patients with mild hypercholesterolemia prefer the use of food supplements since these are perceived to be safer. Here, we investigate the phytochemical profile and cholesterol-lowering potential of Protium heptaphyllum gum resin extract (PHE). Chemical characterization via HPLC-APCI-HRMS2 and…

0301 basic medicineModels MolecularProtein ConformationDrug Evaluation Preclinical030204 cardiovascular system & hematologyPharmacologyPPARαTerpenelcsh:ChemistryPCSK9chemistry.chemical_compound0302 clinical medicineCatalytic DomainSettore BIO/10 - BiochimicaPlant Gumslcsh:QH301-705.5SpectroscopyChromatography High Pressure LiquidFlame IonizationMonacolinChemistryAnticholesteremic AgentsGeneral MedicineComputer Science ApplicationsMolecular Docking SimulationCholesterolPhytochemicalMolecular dockinglipids (amino acids peptides and proteins)Breu brancoStatinmedicine.drug_classHypercholesterolemiaArticleCatalysisGas Chromatography-Mass SpectrometryInorganic Chemistry03 medical and health sciencesNutraceuticalmedicineHumansLovastatinPhysical and Theoretical ChemistryMolecular BiologyOleananeHMGCREnzymatic activityCholesterolPCSK9Organic ChemistryStatinSettore CHIM/08 - Chimica FarmaceuticaTriterpenes030104 developmental biologyhypercholesterolemia; gene expression; HMGCR; PCSK9; PPARα; enzymatic activity; molecular docking; statin; monacolin; breu brancolcsh:Biology (General)lcsh:QD1-999Breu branco; Enzymatic activity; Gene expression; HMGCR; Hypercholesterolemia; Molecular docking; Monacolin; PCSK9; PPARα; StatinLDL receptorDietary SupplementsHepatocytesSettore BIO/14 - FarmacologiaGene expressionHydroxymethylglutaryl-CoA Reductase InhibitorsResins PlantHydrogen
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Niemann-Pick type C2 protein supplementation in experimental non-alcoholic fatty liver disease

2017

BACKGROUND AND AIMS: Hepatic cholesterol deposition drives inflammation and fibrosis in non-alcoholic steatohepatitis (NASH). The Niemann-Pick type C2 (NPC2) protein plays an important role in regulating intracellular cholesterol trafficking and homeostasis. We hypothesized that intravenous NPC2 supplementation reduces cholesterol accumulation, hepatic inflammation and fibrogenesis in a nutritional NASH rat model.METHODS: Rats were fed a high-fat, high-cholesterol (HFHC) diet for four weeks resulting in moderately severe NASH. Animals were treated with intravenous NPC2 or placebo twice weekly for either the last two weeks or the entire four weeks. End-points were liver/body- and spleen/body…

0301 basic medicinePhysiologyGene Expressionlcsh:MedicinePathology and Laboratory MedicineBiochemistrychemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseSterol Regulatory Element Binding ProteinsInnate Immune SystemMultidisciplinarybiologyLiver DiseasesReverse cholesterol transportFatty liverIntracellular Signaling Peptides and ProteinsLipidsCholesterolLiverCytokinesLiver FibrosisFemale030211 gastroenterology & hepatologylipids (amino acids peptides and proteins)Research Articlemedicine.medical_specialtyImmunologyBiological Transport ActiveGastroenterology and HepatologyCollagen Type I03 medical and health sciencesSigns and SymptomsDiagnostic MedicineInternal medicineGeneticsmedicineAnimalsRats WistarGlycoproteinsNutritionInflammationbusiness.industryCholesterollcsh:RBiology and Life Sciencesnutritional and metabolic diseasesMolecular Developmentmedicine.diseaseDietary FatsFibrosisRatsDietCollagen Type I alpha 1 ChainPPAR gammaFatty LiverDisease Models Animal030104 developmental biologyEndocrinologychemistryImmune SystemABCA1LDL receptorbiology.proteinlcsh:QSteatohepatitisCarrier ProteinsbusinessDevelopmental BiologyLipoprotein
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PCSK9-D374Y mediated LDL-R degradation can be functionally inhibited by EGF-A and truncated EGF-A peptides: An in vitro study.

2019

Abstract Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low density lipoprotein receptor (LDLR) through the LDLR epidermal growth factor-like repeat A (EGF-A) domain and induces receptor internalization and degradation. PCSK9 has emerged as a novel therapeutic target for hypercholesterolemia. Clinical studies with PCSK9 inhibiting antibodies have demonstrated strong LDL-c lowering effects, but other therapeutic approaches using small molecule inhibitors for targeting PCSK9 functions may offer supplementary therapeutic options. The aim of our study was to evaluate the effect of synthetic EGF-A analogs on mutated (D374Y) PCSK9-D374Y mediated LDLR degradatio…

0301 basic medicineSmall peptidesmedia_common.quotation_subject030204 cardiovascular system & hematologyDecoy strategyPCSK903 medical and health sciences0302 clinical medicineHumansInternalizationCells Culturedmedia_commonExpression vectorEpidermal Growth FactorChemistryPCSK9PCSK9 InhibitorsTransfectionProprotein convertasePCSK9 inhibitionIn vitroCell biologyEGF-A domain030104 developmental biologyLDLRReceptors LDLLDL receptorMutationKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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Combined B, T and NK Cell Deficiency Accelerates Atherosclerosis in BALB/c Mice.

2016

This study focused on the unique properties of both the Ldlr knockout defect (closely mimicking the human situation) and the BALB/c (C) inbred mouse strain (Th-2 slanted immune response). We generated two immunodeficient strains with severe combined B- and T-cell immunodeficiency with or without a complete lack of natural killer cells to revisit the role of adaptive immune responses on atherogenesis. C-Ldlr-/- Rag1-/- mice, which show severe combined B- and T-cell immunodeficiency and C-Ldlr-/- Rag1-/- Il2rg-/- mice, which combine the T- and B-cell defect with a complete lack of natural killer cells and inactivation of multiple cytokine signalling pathways were fed an atherogenic Western ty…

0301 basic medicineT-Lymphocyteslcsh:MedicineNK cellsAdaptive ImmunityBiochemistryVascular MedicineMicechemistry.chemical_compoundCellular typesReceptorlcsh:ScienceImmunodeficiencyMice KnockoutB-LymphocytesMice Inbred BALB CMultidisciplinarybiologyT CellsImmune cellsAcquired immune systemLipidsPlaque AtheroscleroticKiller Cells NaturalCholesterolPhenotypeWhite blood cellsFemalelipids (amino acids peptides and proteins)Research ArticleCell biologyBlood cellsLipoproteinsImmunologyResearch and Analysis MethodsBALB/cImmune Deficiency03 medical and health sciencesImmune systemmedicineAnimalsImmunohistochemistry TechniquesTriglyceridesMedicine and health sciencesBiology and life sciencesCholesterolMacrophageslcsh:RImmunologic Deficiency SyndromesWild typeProteinsAtherosclerosisbiology.organism_classificationmedicine.diseaseMolecular biologyHistochemistry and Cytochemistry Techniques030104 developmental biologyAnimal cellsReceptors LDLchemistryImmune SystemMutationImmunologyLDL receptorImmunologic TechniquesClinical Immunologylcsh:QClinical MedicinePLoS ONE
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Association of liver steatosis with lipid oversecretion and hypotriglyceridaemia in C57BL/6j mice fed trans-10, cis-12-linoleic acid

2003

AbstractConjugated linoleic acids (CLA) have recently been recognized to reduce body fat and plasma lipids in some animals. This study demonstrated that the steatosis accompanying the fat loss induced by trans-10,cis-12-C18:2 (CLA2) and not cis-9,trans-11-C18:2 (CLA1) isomer in C57BL/6j mice was not due to an alteration of the liver lipoprotein production that was even increased. The 3-fold decrease in plasma triacylglycerol contents and the induction of mRNA expression of low-density lipoprotein receptors concomitantly observed in CLA2-fed mice suggested an increase in the lipoprotein clearance at the level of the liver itself. CLA1 feeding produced similar but attenuated effects on trigly…

030309 nutrition & dieteticsConjugated linoleic acidLiver steatosisLipoproteins VLDLBiochemistrychemistry.chemical_compoundMiceStructural BiologyLipoproteinReceptorComputingMilieux_MISCELLANEOUSchemistry.chemical_classification0303 health sciencesFatty AcidsLiverlipids (amino acids peptides and proteins)Conjugated linoleic acidmedicine.medical_specialtyLinoleic acidBiophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyTriacylglycerolLinoleic Acid03 medical and health sciencesInternal medicineGeneticsmedicineAnimalsLow-density lipoprotein receptorRNA MessengerMolecular BiologyTriglycerides030304 developmental biologyDNA PrimersBase SequenceEsterificationMyocardiumBody WeightRNAFatty acidCell BiologyFatty acidmedicine.diseaseFatty LiverMice Inbred C57BLEndocrinologychemistryLDL receptorSteatosisLipoprotein
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Homozygous familial hypercholesterolemia in Italy: Clinical and molecular features

2020

Abstract Background and aims Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disorder characterized by extremely elevated plasma levels of low density lipoprotein cholesterol (LDL-C) and high risk of premature atherosclerotic cardiovascular disease (ASCVD). HoFH is caused by pathogenic variants in several genes, such as LDLR, APOB and PCSK9, responsible for autosomal dominant hypercholesterolemia (ADH), and LDLRAP1 responsible for autosomal recessive hypercholesterolemia (ARH). Aim of this study was the review of the clinical and molecular features of patients with HoFH identified in Italy from 1989 to 2019. Methods Data were collected from lipid clinics and laboratories, …

Adult0301 basic medicinemedicine.medical_specialtyCandidate geneCandidate geneGenotype-phenotype correlationApolipoprotein BCandidate genes; Genotype-phenotype correlations; Homozygous familial hypercholesterolemia; Pathogenic variantsHomozygous familial hypercholesterolemiaGenotype-phenotype correlationsFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosityCandidate genesHyperlipoproteinemia Type II03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansbiologybusiness.industryPCSK9HomozygoteGenetic disorderPathogenic variantsCandidate genes; Genotype-phenotype correlations; Homozygous familial hypercholesterolemia; Pathogenic variants;medicine.diseasePhenotype030104 developmental biologyEndocrinologyItalyReceptors LDLAutosomal Recessive HypercholesterolemiaMutationLDL receptorbiology.proteinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular Medicinebusiness
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Influence of LDL receptor gene mutations and the R3500Q mutation of the apoB gene on lipoprotein phenotype of familial hypercholesterolemic patients …

2003

Few data are available on genotype-phenotype interactions among familial hypercholesterolemia (FH) patients in South European populations and there are no data about the influence of R3500Q mutation on lipoprotein phenotype compared to low-density lipoprotein receptor (LDLR) mutations. The objective of the study is to analyze the influence of mutations in the LDLR and apolipoprotein B (apoB) genes on lipoprotein phenotype among subjects clinically diagnosed of FH living in East Spain. In all, 113 FH index patients and 100 affected relatives were studied. Genetic diagnosis was carried out following a protocol based on Southern blot and PCR-SSCP analysis. A total of 118 FH subjects could be c…

AdultAdolescentApolipoprotein BHypercholesterolemiaPopulationMutation MissenseFamilial hypercholesterolemiaBiologymedicine.disease_causechemistry.chemical_compoundGeneticsmedicineHumansMissense mutationeducationGenetics (clinical)Apolipoproteins BGeneticsMutationeducation.field_of_studyCholesterolMiddle Agedmedicine.diseaseEuropePhenotypeReceptors LDLchemistryLDL receptorbiology.proteinlipids (amino acids peptides and proteins)LipoproteinEuropean Journal of Human Genetics
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