Search results for "Endoplasmic Reticulum Stre"

showing 10 items of 52 documents

Homocysteine Induces Apoptosis of Human Umbilical Vein Endothelial Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

2017

Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspa…

0301 basic medicineAgingArticle SubjectApoptosis030204 cardiovascular system & hematologyTransfectionBiochemistryUmbilical vein03 medical and health sciences0302 clinical medicineRisk FactorsHuman Umbilical Vein Endothelial CellsHumanslcsh:QH573-671Protein kinase AEndoplasmic Reticulum Chaperone BiPHomocysteinebiologylcsh:CytologyKinaseEndoplasmic reticulumCytochrome cCell BiologyGeneral MedicineEndoplasmic Reticulum StressMitochondriaCell biology030104 developmental biologyApoptosiscardiovascular systemUnfolded protein responsebiology.proteinPhosphorylationResearch ArticleOxidative Medicine and Cellular Longevity
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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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The secreted protein acidic and rich in cysteine is a critical mediator of cell death program induced by WIN/TRAIL combined treatment in osteosarcoma…

2015

Abstract Secreted protein acidic and rich in cysteine (SPARC) is a multi-functional protein which modulates cell-cell and cell-matrix interactions. In cancer cells, SPARC behaves as a tumor promoter in a number of tumors, but it can also act as a tumor suppressor factor. Our previous results showed that the synthetic cannabinoid WIN55,212-2 (WIN), a potent cannabinoid receptor agonist, is able to sensitize osteosarcoma MG63 cells to TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis which is accompanied with endoplasmic reticulum (ER)-stress induction and the increase in autophagic markers. In the present investigation, we studied the role of SPARC in WIN/TRAIL-induced apoptosi…

0301 basic medicineCancer ResearchProgrammed cell deathCell SurvivalMorpholinesCellSPARC cannabinoids osteosarcoma apoptosis caspase-8 activationApoptosisBone NeoplasmsBiologyNaphthalenesTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences0302 clinical medicineProtein DomainsSettore BIO/10 - BiochimicaCell Line TumormedicineCytotoxic T cellHumansOsteonectinGene SilencingCaspase 8OsteosarcomaOncogeneCell DeathEndoplasmic reticulumCell MembraneCell cycleEndoplasmic Reticulum StressCell biologyBenzoxazines030104 developmental biologymedicine.anatomical_structureOncologyApoptosis030220 oncology & carcinogenesisCancer cellRNA InterferenceInternational journal of oncology
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Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

2017

Abstract Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ…

0301 basic medicineCancer ResearchTime FactorsCOPZ1ApoptosisCOPZ1Thyroid cancerThyroid NeoplasmThyroidRNAi TherapeuticCell death; COPZ1; Non-oncogene addiction; Thyroid carcinoma; Animals; Apoptosis; Autophagy; Cell Line Tumor; Cell Survival; Coatomer Protein; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation Neoplastic; Humans; Mice Nude; RNA Interference; Signal Transduction; Thyroid Neoplasms; Time Factors; Transfection; Tumor Burden; Unfolded Protein Response; Xenograft Model Antitumor Assays; RNAi Therapeutics; Oncology; Cancer ResearchEndoplasmic Reticulum StressOncogene AddictionTumor BurdenGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyFemaleRNA InterferenceNon-oncogene addictionHumanSignal TransductionCell deathProgrammed cell deathXenograft Model Antitumor AssayTime FactorCell SurvivalMice NudeBiologyTransfectionCoatomer ProteinThyroid carcinomaThyroid carcinoma03 medical and health sciencesCell Line TumorAutophagymedicineAnimalsHumansThyroid NeoplasmsEndoplasmic Reticulum StreAnimalAutophagyApoptosimedicine.diseaseXenograft Model Antitumor AssaysRNAi Therapeutics030104 developmental biologyImmunologyUnfolded Protein ResponseCancer researchUnfolded protein response
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Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer.

2020

Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signaling to promote cell survival in an inflammatory and hypoxic microenvironment in order to maintain/expand tumor phenotype. The administration of tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy in different malignancies at advanced stages. There are important interrelationships between cell stress, redox status, mitochondrial function, metabolism and cellular signali…

0301 basic medicineCell deathCell signalingClinical BiochemistryPGC-1αApoptosisReview ArticleBiochemistryReceptor tyrosine kinase03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsAutophagyTumor MicroenvironmentHumansProtein kinase AProtein kinase Blcsh:QH301-705.5Protein Kinase InhibitorsPI3K/AKT/mTOR pathwaylcsh:R5-920biologyOrganic ChemistryMitochondria030104 developmental biologylcsh:Biology (General)Redox statusCancer cellbiology.proteinCancer researchEndoplasmic reticulum stressmTORSignal transductionlcsh:Medicine (General)Tyrosine kinaseProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryRedox biology
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Oxidative and endoplasmic reticulum stress is impaired in leukocytes from metabolically unhealthy vs healthy obese individuals.

2017

BACKGROUND: Oxidative stress and inflammation are related to obesity, but the influence of metabolic disturbances on these parameters and their relationship with endoplasmic reticulum (ER) stress is unknown. Therefore, this study was performed to evaluate whether metabolic profile influences ER and oxidative stress in an obese population with/without comorbidities. SUBJECTS AND METHODS: A total of 113 obese patients were enrolled in the study; 29 were metabolically healthy (MHO), 53 were metabolically abnormal (MAO) and 31 had type 2 diabetes (MADO). We assessed metabolic parameters, proinflammatory cytokines (TNF alpha and IL-6), mitochondrial and total reactive oxygen species (ROS) produc…

0301 basic medicineMaleEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Blood Pressuremedicine.disease_causeBody Mass Index0302 clinical medicineLeukocytesEndoplasmic Reticulum Chaperone BiPchemistry.chemical_classificationMetabolic SyndromeNutrition and DieteticsMiddle AgedEndoplasmic Reticulum StressCytokinesFemalemedicine.symptomOxidation-ReductionAdultmedicine.medical_specialtyBlotting Western030209 endocrinology & metabolismInflammationOxidative phosphorylation03 medical and health sciencesYoung AdultInsulin resistanceInternal medicinemedicineHumansObesityAgedDyslipidemiasInflammationReactive oxygen speciesObesity Metabolically Benignbusiness.industryEndoplasmic reticulummedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologychemistryMetabolic syndromeInsulin ResistancebusinessReactive Oxygen SpeciesBody mass indexOxidative stressInternational journal of obesity (2005)
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Protein misfolding, amyotrophic lateral sclerosis and guanabenz: Protocol for a phase II RCT with futility design (ProMISe trial)

2017

IntroductionRecent studies suggest that endoplasmic reticulum stress may play a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS) through an altered regulation of the proteostasis, the cellular pathway-balancing protein synthesis and degradation. A key mechanism is thought to be the dephosphorylation of eIF2α, a factor involved in the initiation of protein translation. Guanabenz is an alpha-2-adrenergic receptor agonist safely used in past to treat mild hypertension and is now an orphan drug. A pharmacological action recently discovered is its ability to modulate the synthesis of proteins by the activation of translational factors preventing misfolded protein accumula…

0301 basic medicineOncologyPathologyamyotrophic lateral sclerosisamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; adrenergic alpha-2 receptor agonist s; age of onset; amyotrophic lateral sclerosis; disease progression; double-blind method; endoplasmic reticulum stress; guanabenz; humans; italy; medical futility; neuroprotective agents; proteostasis deficienciesamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Medicine (all)randomized clinical trial guanabenzHelsinki declaration0302 clinical medicineProtocolAdrenergic alpha-2 Receptor Agonists1506Amyotrophic lateral sclerosisAge of OnsetGuanabenzMedicine (all)amyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein responseNeurodegenerationamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response;amyotrophic lateral sclerosis; guanabenz; motor neurone disease; neuromuscular disease; randomized clinical trial; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis DeficienciesGeneral Medicineunfolded protein responseEndoplasmic Reticulum StressRiluzoleNeuroprotective AgentsNeurologyTolerabilityItalyDisease Progression1713GuanabenzMedical Futilitymedicine.drugmedicine.medical_specialtyamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis Deficiencies; Medicine (all)Neuroprotection03 medical and health sciencesmotor neurone diseaseDouble-Blind MethodInternal medicinemedicineHumansProteostasis Deficienciesbusiness.industryAmbientaleneuromuscular diseaserandomized clinical trialmedicine.diseaseClinical trial030104 developmental biologybusiness030217 neurology & neurosurgery
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Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases

2021

Several studies have shown that some rare respiratory diseases, such as alpha-1 antitrypsin deficiency (AATD), idiopathic pulmonary fibrosis (IPF), cystic fibrosis (CF), and primary ciliary dyskinesia (PCD) present oxidative stress (OS) and endoplasmic reticulum (ER) stress. Their involvement in these pathologies and the use of antioxidants as therapeutic agents to minimize the effects of OS are discussed in this review.

0301 basic medicinePathologymedicine.medical_specialtylcsh:Medicineprimary ciliary dyskinesiaReviewrare respiratory diseasesmedicine.disease_causeCystic fibrosiscystic fibrosis03 medical and health sciencesIdiopathic pulmonary fibrosis0302 clinical medicineotorhinolaryngologic diseasesmedicineoxidative stressRespiratory systemPrimary ciliary dyskinesiaAlpha 1-antitrypsin deficiencybusiness.industryEndoplasmic reticulumlcsh:RGeneral Medicineidiopathic pulmonary fibrosismedicine.diseaserespiratory tract diseases030104 developmental biologyAlpha-1 antitrypsin deficiency030220 oncology & carcinogenesisendoplasmic reticulum stressantioxidant therapiesbusinessOxidative stressJournal of Clinical Medicine
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Anticancer metal drugs and immunogenic cell death

2016

Conventional chemotherapeutics, but also innovative precision anticancer compounds, are commonly perceived to target primarily the cancer cell compartment. However, recently it was discovered that some of these compounds can also exert immunomodulatory activities which might be exploited to synergistically enhance their anticancer effects. One specific phenomenon of the interplay between chemotherapy and the anticancer immune response is the so-called “immunogenic cell death” (ICD). ICD was discovered based on a vaccination effect exerted by cancer cells dying from pretreatment with certain chemotherapeutics, termed ICD inducers, in syngeneic transplantation mouse models. Interestingly, onl…

0301 basic medicineProgrammed cell deathOrganoplatinum Compoundsmedicine.medical_treatmentAntineoplastic AgentsPharmacologyBiochemistryAntineoplastic AgentInorganic ChemistryMice03 medical and health sciences0302 clinical medicineImmune systemCancer immunotherapyNeoplasmsmedicineAnimalsHumansEndoplasmic Reticulum StreCisplatinChemotherapyCell DeathAnimalChemistryOrganoplatinum CompoundEndoplasmic Reticulum Stress3. Good healthOxaliplatin030104 developmental biologyAnticancer metal drugSettore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesisCancer cellUnfolded protein responseImmunogenic cell deathCisplatinReactive Oxygen SpecieReactive Oxygen SpeciesImmunogenic cell deathHumanmedicine.drugJournal of Inorganic Biochemistry
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Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress

2016

Protein homeostasis in cells, proteostasis, is maintained through several integrated processes and pathways and its dysregulation may mediate pathology in many diseases including Duchenne muscular dystrophy (DMD). Oxidative stress, heat shock proteins, endoplasmic reticulum (ER) stress and its response, i.e. unfolded protein response (UPR), play key roles in proteostasis but their involvement in the pathology of DMD are largely unknown. Moreover, exercise and activin receptor IIB blocking are two strategies that may be beneficial to DMD muscle, but studies to examine their effects on these proteostasis pathways are lacking. Therefore, these pathways were examined in the muscle of mdx mice, …

0301 basic medicineX-Box Binding Protein 1Activin Receptors Type IIEukaryotic Initiation Factor-2MyostatinUPRBiochemistryMiceeIF-2 KinaseThioredoxinsSirtuin 1ENDOPLASMIC-RETICULUM STRESSDISULFIDE-ISOMERASEPhosphorylationta315Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsIN-VIVOta3141Activin receptorMOUSE MODELER STRESSEndoplasmic Reticulum Stress3. Good healthmedicine.anatomical_structuremyostatinPRESERVES MUSCLE FUNCTIONER-stressSKELETAL-MUSCLEmdxSignal TransductionEXPRESSIONmedicine.medical_specialtyXBP1MDX MICEBiologyProtein Serine-Threonine Kinases03 medical and health sciencesPhysiology (medical)Internal medicineHeat shock proteinPhysical Conditioning AnimalEndoribonucleasesmedicineAnimalsHumansRNA MessengerMuscle SkeletalSkeletal muscleMyostatinGENEActivating Transcription Factor 6Immunoglobulin Fc FragmentsMuscular Dystrophy DuchenneDisease Models Animal030104 developmental biologyProteostasisEndocrinologyGene Expression RegulationUnfolded protein responsebiology.proteinMice Inbred mdxProteostasisUnfolded Protein Response3111 BiomedicineCarrier ProteinsACVR2B
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