Search results for "ATF6"

showing 10 items of 13 documents

The cytoprotective protein MANF promotes neuronal survival independently from its role as a GRP78 cofactor

2021

Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER)-stress-regulated protein exhibiting cytoprotective properties through a poorly understood mechanism in various in vitro and in vivo models of neuronal and non-neuronal damage. Although initially characterized as a secreted neurotrophic factor for midbrain dopamine neurons, MANF has recently gained more interest for its intracellular role in regulating the ER homeostasis, including serving as a cofactor of the chaperone glucose-regulated protein 78 (GRP78). We aimed for a better understanding of the neuroprotective mechanisms of MANF. Here we show for the first time that MANF promotes the survival of …

0301 basic medicineBiFC bimolecular fluorescence complementationMST microscale thermophoresisPDIA1 protein disulfide isomerase family A member 1ApoptosisNEUROTROPHIC FACTOR MANFEndoplasmic ReticulumBiochemistryprotein-protein interactionMiceBimolecular fluorescence complementationUPR unfolded protein responseENDOPLASMIC-RETICULUM STRESSMesencephalonNeurotrophic factorsInsulin-Secreting CellsProtein Interaction MappingBINDINGCOMPREHENSIVE RESOURCEATF6unfolded protein response (UPR)PDIA6 protein disulfide isomerase family A member 6PPIs protein-protein interactionsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsNPTN neuroplastinbiologyChemistryapoptosisunfolded protein responsedopamine neurons3. Good healthCell biologyGDNF glial cell line–derived neurotrophic factorIRE1-ALPHASBD substrate-binding domainendoplasmic reticulum stressMANF mesencephalic astrocyte-derived neurotrophic factorTm tunicamycinneuroprotectionResearch ArticleProtein BindingSignal TransductionGRP78Protein Disulfide-Isomerase FamilyCell SurvivalTH tyrosine hydroxylasePrimary Cell CultureSCG superior cervical ganglionProtein Disulfide-IsomerasesIRE1 inositol-requiring enzyme 1ER-STRESSER endoplasmic reticulum03 medical and health sciencesohjelmoitunut solukuolemaC-MANF C-terminal domain of MANFCSPs chemical shift perturbationsAnimalsHumansHSP70 Heat-Shock ProteinsNerve Growth FactorsNBD nucleotide-binding domainNMR nuclear magnetic resonanceMolecular Biology030102 biochemistry & molecular biologyBIPATF6Dopaminergic NeuronsGene Expression ProfilingBinding proteinneuronal cell deathDISSOCIATIONCell BiologyNEI nucleotide exchange inhibitorEmbryo MammalianadenosiinitrifosfaattiATPhermosolutmesencephalic astrocyte-derived neurotrophic factorprotein–protein interactionPERK protein kinase RNA-like ER kinaseHEK293 Cells030104 developmental biologyGene Expression RegulationChaperone (protein)Tg thapsigarginbiology.proteinUnfolded protein responseAP-MS affinity purification mass spectrometry1182 Biochemistry cell and molecular biologyGFP-SH SH-tagged GFPendoplasmic reticulum stress (ER stress)DA dopaminemesencephalic astrocyte-derived neurotrophic factor (MANF)proteiinitNeuroplastin
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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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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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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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Isoquercitrin and polyphosphate co-enhance mineralization of human osteoblast-like SaOS-2 cells via separate activation of two RUNX2 cofactors AFT6 a…

2014

Isoquercitrin, a dietary phytoestrogen, is a potential stimulator of bone mineralization used for prophylaxis of osteoporotic disorders. Here we studied the combined effects of isoquercitrin, a cell membrane permeable 3-O-glucoside of quercetin, and polyphosphate [polyP], a naturally occurring inorganic polymer inducing bone formation, on mineralization of human osteoblast-like SaOS-2 cells. Both compounds isoquercitrin and polyP induce at non-toxic concentrations the mineralization process of SaOS-2 cells. Co-incubation experiments revealed that isoquercitrin (at 0.1 and 0.3μM), if given simultaneously with polyP (as Ca(2+) salt; at 3, 10, 30 and 100μM) amplifies the mineralization-enhanci…

Activating transcription factorBiochemistryProto-Oncogene Protein c-ets-103 medical and health sciences0302 clinical medicineCalcification PhysiologicPolyphosphatesCell Line TumormedicineHumansSaos-2 cells030304 developmental biologyPharmacology0303 health sciencesOsteoblastsbiologyATF6OsteoblastDrug SynergismActivating Transcription Factor 6RUNX2medicine.anatomical_structureBiochemistryGene Expression Regulation030220 oncology & carcinogenesisOsteocalcinbiology.proteinAlkaline phosphataseCalciumQuercetinSignal transductionBiochemical pharmacology
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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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Ethanol-Mediated Stress Promotes Autophagic Survival and Aggressiveness of Colon Cancer Cells via Activation of Nrf2/HO-1 Pathway

2019

Epidemiological studies suggest that chronic alcohol consumption is a lifestyle risk factor strongly associated with colorectal cancer development and progression. The aim of the present study was to examine the effect of ethanol (EtOH) on survival and progression of three different colon cancer cell lines (HCT116, HT29, and Caco-2). Our data showed that EtOH induces oxidative and endoplasmic reticulum (ER) stress, as demonstrated by reactive oxygen species (ROS) and ER stress markers Grp78, ATF6, PERK and, CHOP increase. Moreover, EtOH triggers an autophagic response which is accompanied by the upregulation of beclin, LC3-II, ATG7, and p62 proteins. The addition of the antioxidant N-acetyl…

Cancer Researchendocrine systemautophagyHO-1Colon cancer cellmedicine.disease_causelcsh:RC254-282ArticleNrf2Downregulation and upregulationSettore BIO/10 - Biochimicamedicinechemistry.chemical_classificationReactive oxygen speciesATF6Endoplasmic reticulumAutophagylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHeme oxygenaseOncologychemistryCancer researchUnfolded protein responseER strecolon cancer cellsethanolMMPsER stressOxidative stressCancers
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Consensus guidelines for the detection of immunogenic cell death

2014

Apoptotic cells have long been considered as intrinsically tolerogenic or unable to elicit immune responses specific for dead cell-associated antigens. However, multiple stimuli can trigger a functionally peculiar type of apoptotic demise that does not go unnoticed by the adaptive arm of the immune system, which we named "immunogenic cell death" (ICD). ICD is preceded or accompanied by the emission of a series of immunostimulatory damage-associated molecular patterns (DAMPs) in a precise spatiotemporal configuration. Several anticancer agents that have been successfully employed in the clinic for decades, including various chemotherapeutics and radiotherapy, can elicit ICD. Moreover, defect…

HSV-1 herpes simplex virus type IΔψm mitochondrial transmembrane potentialmedicine.medical_treatmentDAMP damage-associated molecular patterndetectionFLT3LG fms-related tyrosine kinase 3 ligandReviewmember 3calreticulinEukaryotic translation initiation factor 2ARFP red fluorescent protein0302 clinical medicineMOMP mitochondrial outer membrane permeabilizationImmunology and AllergyGFP green fluorescent proteinHMGB10303 health scienceseducation.field_of_studyToll-like receptorBAK1 BCL2-antagonist/killer 1H2B histone 2Bendoplasmic reticulum stre3. Good healthBAX BCL2-associated X proteinXBP1 X-box binding protein 1cell deathOncologyPDIA3 protein disulfide isomerase family A030220 oncology & carcinogenesisendoplasmic reticulum stressImmunogenic cell deathHSP heat shock proteinimmunotherapyTLR Toll-like receptorautophagyATF6 activating transcription factor 6ImmunologyICD immunogenic cell deathEIF2A eukaryotic translation initiation factor 2AGuidelinesBiologyBCL2 B-cell CLL/lymphoma 2 proteinER endoplasmic reticulumPI propidium iodideATP release03 medical and health sciencesImmune systemimmunogenicmedicineIFN interferonAntigen-presenting celleducation030304 developmental biologyCALR calreticulinDamage-associated molecular patternImmunotherapyCTL cytotoxic T lymphocyteHMGB1 high mobility group box 1IL interleukinG3BP1 GTPase activating protein (SH3 domain) binding protein 1APC antigen-presenting cellCancer cellImmunologyDiOC6(3) 33′-dihexyloxacarbocyanine iodideDAPI 4′6-diamidino-2-phenylindoleOncoImmunology
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Does Metformin Modulate Endoplasmic Reticulum Stress and Autophagy in Type 2 Diabetic Peripheral Blood Mononuclear Cells?

2018

Since type 2 diabetes (T2D) is associated with oxidative stress and metformin has been shown to exert a protective role against the said stress, we wondered whether metformin treatment might also modulate endoplasmic reticulum (ER) stress and autophagy in leukocytes of T2D patients. We studied 53 T2D patients (37 of whom had been treated with metformin 1700 mg for at least 1 year) and 30 healthy volunteers. Leukocytes from both groups of T2D patients exhibited increased protein levels of 78-kDa glucose-regulated protein (GRP78) with respect to controls, whereas activating transcription factor 6 (ATF6) was enhanced specifically in nonmetformin-treated T2D, and (s-xbp1) and phosphorylated euk…

Male0301 basic medicinemedicine.medical_specialtyendocrine system diseasesPhysiologyClinical BiochemistryAdministration OralType 2 diabetesBiologymedicine.disease_causeBiochemistry03 medical and health sciencesInternal medicineAutophagymedicineHumansEndoplasmic Reticulum Chaperone BiPMolecular BiologyGeneral Environmental ScienceDose-Response Relationship DrugATF6Endoplasmic reticulumAutophagynutritional and metabolic diseasesCell BiologyBECN1Middle AgedEndoplasmic Reticulum Stressmedicine.diseaseMetforminMetforminOxidative StressCross-Sectional Studies030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Leukocytes MononuclearUnfolded protein responseGeneral Earth and Planetary SciencesFemaleOxidative stressmedicine.drugAntioxidants & Redox Signaling
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