Search results for "Endoplasmic reticulum stre"

showing 10 items of 52 documents

Impact of polymer-modified gold nanoparticles on brain endothelial cells: exclusion of endoplasmic reticulum stress as a potential risk factor

2016

A library of polymer-coated gold nanoparticles (AuNPs) differing in size and surface modifications was examined for uptake and induction of cellular stress responses in the endoplasmic reticulum (ER stress) in human brain endothelial cells (hCMEC/D3). ER stress is known to affect the physiology of endothelial cells (ECs) and may lead to inflammation or apoptosis. Thus, even if applied at non-cytotoxic concentrations ER stress caused by nanoparticles should be prevented to reduce the risk of vascular diseases and negative effects on the integrity of barriers (e.g. blood-brain barrier). We exposed hCMEC/D3 to twelve different AuNPs (three sizes: 18, 35, and 65 nm, each with four surface-modif…

0301 basic medicineXBP1BiPCell SurvivalPolymersBiomedical EngineeringMetal NanoparticlesApoptosis02 engineering and technologyBiologyEndoplasmic ReticulumToxicologyArticleCell LineProinflammatory cytokine03 medical and health sciencescell stressDownregulation and upregulationRisk FactorsHeat shock proteinAnimalsHumansHSP70 Heat-Shock ProteinsParticle SizeHeat-Shock ProteinsATF6Endoplasmic reticulumInterleukin-8ATF4Endothelial CellsMembrane Proteinsunfolded protein responseEndoplasmic Reticulum Stress021001 nanoscience & nanotechnologyQPActivating Transcription Factor 4Cell biology030104 developmental biologyBlood-Brain Barriertight junction proteinsImmunologyUnfolded protein responseGold0210 nano-technologyTranscription Factor CHOPNanotoxicology
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The Mitochondria-Targeted Antioxidant MitoQ Modulates Mitochondrial Function and Endoplasmic Reticulum Stress in Pancreatic β Cells Exposed to Hyperg…

2019

Background/aims Mitochondria-targeted antioxidants such as mitoquinone (MitoQ) have demonstrated protective effects against oxidative damage in several diseases. The increase in reactive oxygen species (ROS) production during glucose metabolism in β cells can be exacerbated under hyperglycaemic conditions such as type 2 diabetes (T2D), thus contributing to β cell function impairment. In the present work, we aimed to evaluate the effect of MitoQ on insulin secretion, oxidative stress, endoplasmic reticulum (ER) stress and nuclear factor kappa B (NFκB) signalling in a pancreatic β cell line under normoglycaemic (NG, 11.1 mM glucose), hyperglycaemic (HG, 25 mM glucose) and lipidic (palmitic ac…

0301 basic medicinemedicine.medical_specialtyPhysiologyUbiquinoneCarbohydrate metabolismmedicine.disease_causeMitoQlcsh:PhysiologyPancreatic β cellsAntioxidantsProinflammatory cytokinelcsh:Biochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOrganophosphorus CompoundsInternal medicineCell Line TumorInsulin-Secreting CellsmedicineAnimalslcsh:QD415-436chemistry.chemical_classificationReactive oxygen speciesMitoQlcsh:QP1-981Endoplasmic reticulumGlutathioneEndoplasmic Reticulum StressType 2 DiabetesMitochondriaRatsOxidative Stress030104 developmental biologyEndocrinologyGlucosechemistry030220 oncology & carcinogenesisHyperglycemiaUnfolded protein responseER stressMitochondrial dysfunctionReactive Oxygen SpeciesOxidative stressSignal Transduction
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NUPR1 protects liver from lipotoxic injury by improving the endoplasmic reticulum stress response

2021

AbstractBackground and AimsNon-alcoholic fatty liver disease and related hepatic syndromes affect up to one third of the adult population. The molecular mechanisms underlying NAFL etiology remain elusive. Nuclear Protein 1 (NUPR1) expression increases upon cell injury in all organs and recently we report its active participation in the activation of the Unfolded Protein Response (UPR). The UPR typically maintains protein homeostasis, but downstream mediators of the pathway regulate metabolic functions, including lipid metabolism. NUPR1 and UPR increase have been reported in obesity and liver pathologies and the goal of this study was to investigate the roles of NUPR1 in this context.Methods…

0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaPPAR-a signalling UPRPeroxisome proliferator-activated receptorContext (language use)UPRDiet High-FatBiochemistry03 medical and health sciencesLiver diseaseMice0302 clinical medicineInternal medicineCell Line TumorGeneticsmedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationbusiness.industryEndoplasmic reticulumFatty liverNASHLipid metabolismlipotoxicitymedicine.diseaseEndoplasmic Reticulum StressLipid MetabolismNeoplasm Proteins030104 developmental biologyEndocrinologychemistryLipotoxicityLiverNAFLKnockout mouseUnfolded protein responseUnfolded Protein ResponsePPAR-a signallingSteatosisSteatohepatitisbusiness030217 neurology & neurosurgeryNUPR1Biotechnology
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Metabolic syndrome enhances endoplasmic reticulum, oxidative stress and leukocyte–endothelium interactions in PCOS

2017

Polycystic ovary syndrome (PCOS) is associated with insulin resistance, which can lead to metabolic syndrome (MetS). Oxidative stress and leukocyte-endothelium interactions are related to PCOS. Our aim was to evaluate whether the presence of MetS in PCOS patients can influence endoplasmic reticulum (ER) and oxidative stress and leukocyte-endothelium interactions.This was a prospective controlled study conducted in an academic medical center. The study population consisted of 148 PCOS women (116 without/32 with MetS) and 112 control subjects (87 without / 25 with MetS). Metabolic parameters, reactive oxygen species (ROS) production, ER stress markers (GRP78, sXBP1, ATF6), leukocyte-endotheli…

0301 basic medicinemedicine.medical_specialtyXBP1Endocrinology Diabetes and Metabolism030209 endocrinology & metabolismBiologymedicine.disease_cause03 medical and health sciences0302 clinical medicineEndocrinologyInsulin resistanceInternal medicineCell AdhesionLeukocytesmedicineHumansProspective StudiesEndoplasmic Reticulum Chaperone BiPMetabolic SyndromeInterleukin-6ATF6Endoplasmic Reticulum StressIntercellular Adhesion Molecule-1medicine.diseasePolycystic ovaryOxidative Stress030104 developmental biologyEndocrinologyUnfolded protein responseHomeostatic model assessmentCytokinesFemaleEndothelium VascularMetabolic syndromeReactive Oxygen SpeciesCell Adhesion MoleculesOxidative stressPolycystic Ovary SyndromeMetabolism
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Insulin Dissociates the Effects of Liver X Receptor on Lipogenesis, Endoplasmic Reticulum Stress, and Inflammation

2016

IF 4.258; International audience; Diabetes is characterized by increased lipogenesis as well as increased endoplasmic reticulum (ER) stress and inflammation. The nuclear hormone receptor liver X receptor (LXR) is induced by insulin and is a key regulator of lipid metabolism. It promotes lipogenesis and cholesterol efflux, but suppresses endoplasmic reticulum stress and inflammation. The goal of these studies was to dissect the effects of insulin on LXR action. We used antisense oligonucleotides to knock down Lxr alpha in mice with hepatocytespecific deletion of the insulin receptor and their controls. We found, surprisingly, that knock-out of the insulin receptor and knockdown of Lxr alpha …

0301 basic medicinemedicine.medical_treatmentLipid-metabolismResistanceBiochemistryHepatitisMESH: HepatitisMESH: Endoplasmic Reticulum Stresspolycyclic compoundsInsulinGene-expressionPhospholipidsLiver X ReceptorsMice KnockoutbiologyMESH : Gene Expression RegulationFatty-acid synthesisfood and beveragesEndoplasmic Reticulum StressOrphan Nuclear ReceptorsCultured-cellsLipidsMESH: Gene Expression RegulationMESH : Endoplasmic Reticulum StressMessenger-rnaLiverMESH: Orphan Nuclear ReceptorsGene Knockdown TechniquesLipogenesisFemalelipids (amino acids peptides and proteins)Signal Transductionliver X receptormedicine.medical_specialtyLxr-alphaMice Transgenicdigestive systemPhospholipid transfer proteinGene Expression Regulation Enzymologic03 medical and health sciencesInsulin resistanceMESH : HepatitisLysophosphatidylcholine acyltransferaseInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyLiver X receptorMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCrosses GeneticLipogenesisEndoplasmic reticulumInsulinElement-binding protein-1cMESH : LiverCell Biologymedicine.diseaseMESH : Orphan Nuclear ReceptorsReceptor InsulinMice Inbred C57BLInsulin receptor030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Gene Expression RegulationNuclear receptorbiology.proteinUnfolded protein responseInsulin ResistanceMESH: Liver
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Pinitol alleviates systemic inflammatory cytokines in human obesity by a mechanism involving unfolded protein response and sirtuin 1

2017

Summary Background & aims It is known that pinitol acts as a mediator of the insulin-signaling pathway, though little is known about its anti-inflammatory effect in human obesity. Therefore, this study aimed to evaluate the effect of pinitol on peripheral blood mononuclear cells (PBMCs) and visceral (VAT) and subcutaneous adipose tissues (SAT), focusing on the involvement of endoplasmic reticulum (ER) stress and sirtuin 1 (SIRT1). Methods In the intervention study, thirteen obese subjects consumed a pinitol-enriched beverage (PEB) for 12 weeks. In the ex vivo study, a biopsy of VAT and SAT was removed from thirty-four obese patients and incubated with D-pinitol for 48 h. Results The consump…

AdultMale0301 basic medicinemedicine.medical_specialtyAnti-Inflammatory AgentsAdipose tissueInflammationWhite adipose tissueCritical Care and Intensive Care MedicineProinflammatory cytokine03 medical and health scienceschemistry.chemical_compoundSirtuin 1Internal medicineHumansMedicineObesityAgedInflammationNutrition and DieteticsPinitolbiologybusiness.industryATF6Sirtuin 1Middle AgedEndoplasmic Reticulum Stress030104 developmental biologyEndocrinologyAdipose TissuechemistryLeukocytes MononuclearUnfolded Protein ResponseUnfolded protein responsebiology.proteinCytokinesFemalemedicine.symptombusinessInositolClinical Nutrition
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Role of Endoplasmic Reticulum and Oxidative Stress Parameters in the Pathophysiology of Disease-Related Malnutrition in Leukocytes of an Outpatient P…

2019

Cellular pathways such as inflammation or oxidative stress are the cause and triggers of disease-related malnutrition (DRM), but the influence of these markers on endoplasmic reticulum (ER) stress is unknown. The objective of this study was to analyze the relationship between mitochondrial function and ER stress parameters in a DRM population. The study population was composed of 82 outpatient subjects, of whom 45 were diagnosed with DRM and 37 were confirmed to be normonourished according to the American Society for Parenteral and Enteral Nutrition ASPEN criteria. We evaluated anthropometrical and biochemical parameters, pro-inflammatory cytokines in serum. Oxidative and ER stress markers …

AdultMale0301 basic medicinemedicine.medical_specialtyPopulationNutritional Statuslcsh:TX341-641InflammationOxidative phosphorylationEndoplasmic Reticulummedicine.disease_cause03 medical and health sciences0302 clinical medicinemitochondrial functionInternal medicineOutpatientsdisease-related malnutritionLeukocytesmedicineHumans030212 general & internal medicineeducationoutpatient populationAgededucation.field_of_study030109 nutrition & dieteticsNutrition and DieteticsAnthropometryATF6business.industryBrief ReportEndoplasmic reticulumMalnutritionMiddle AgedOxidative StressEndocrinologyinflammationendoplasmic reticulum stressUnfolded protein responseCytokinesFemaleSignal transductionmedicine.symptombusinesslcsh:Nutrition. Foods and food supplyOxidative stressFood ScienceNutrients
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Disease-associated polymorphisms in ERAP1 do not alter endoplasmic reticulum stress in patients with ankylosing spondylitis

2014

The mechanism by which human leukocyte antigen B27 (HLA-B27) contributes to ankylosing spondylitis (AS) remains unclear. Genetic studies demonstrate that association with and interaction between polymorphisms of endoplasmic reticulum aminopeptidase 1 (ERAP1) and HLA-B27 influence the risk of AS. It has been hypothesised that ERAP1-mediated HLA-B27 misfolding increases endoplasmic reticulum (ER) stress, driving an interleukin (IL) 23-dependent, pro-inflammatory immune response. We tested the hypothesis that AS-risk ERAP1 variants increase ER-stress and concomitant pro-inflammatory cytokine production in HLA-B27(+) but not HLA-B27(-) AS patients or controls. Forty-nine AS cases and 22 healthy…

AdultMaleAnkylosing Spondylitismedicine.medical_treatmentImmunologyInflammationSingle-nucleotide polymorphismDiseaseBiologyERAP1AminopeptidasesPolymorphism Single NucleotideMinor Histocompatibility AntigensYoung AdultGene expressionGeneticsmedicineHumansSpondylitis AnkylosingERAP1 Ankylosing SpondylitisEndoplasmic Reticulum Chaperone BiPSpondylitisHLA-B27 AntigenGenetics (clinical)InflammationAnkylosing spondylitisEndoplasmic reticulumMiddle AgedEndoplasmic Reticulum Stressmedicine.diseaseCytokineImmunologyFemalemedicine.symptomGenes & Immunity
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Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
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