Search results for " cell death"

showing 10 items of 646 documents

Golgi Fragmentation in Neurodegenerative Diseases: Is There a Common Cause?

2019

In most mammalian cells, the Golgi complex forms a continuous ribbon. In neurodegenerative diseases, the Golgi ribbon of a specific group of neurons is typically broken into isolated elements, a very early event which happens before clinical and other pathological symptoms become evident. It is not known whether this phenomenon is caused by mechanisms associated with cell death or if, conversely, it triggers apoptosis. When the phenomenon was studied in diseases such as Parkinson’s and Alzheimer’s or amyotrophic lateral sclerosis, it was attributed to a variety of causes, including the presence of cytoplasmatic protein aggregates, malfunctioning of intracellular traffic and/or alterations i…

intracellular transportProgrammed cell deathGolgi ApparatusReviewProtein aggregationBiologyProtein Aggregation Pathologicalsymbols.namesakeMicemedicineAnimalsHumansAmyotrophic lateral sclerosisFragmentation (cell biology)Cytoskeletonlcsh:QH301-705.5NeuronscytoskeletonNeurodegenerative DiseasesGeneral MedicineGolgi apparatusmedicine.diseaseprotein aggregatesGolgi complexlcsh:Biology (General)ApoptosissymbolsNeuroscienceIntracellularCells
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Osteoclast Immunosuppressive Effects in Multiple Myeloma: Role of Programmed Cell Death Ligand 1

2018

Immunomodulatory drugs and monoclonal antibody-based immunotherapies have significantly improved the prognosis of the patients with multiple myeloma (MM) in the recent years. These new classes of reagents target malignant plasma cells (PCs) and further modulate the immune microenvironment, which prolongs anti-MM responses and may prevent tumor occurrence. Since MM remains an incurable cancer for most patients, there continues to be a need to identify new tumor target molecules and investigate alternative cellular approaches using gene therapeutic strategies and novel treatment mechanisms. Osteoclasts (OCs), as critical multi-nucleated large cells responsible for bone destruction in >80% …

lcsh:Immunologic diseases. Allergy0301 basic medicineCarcinogenesisAngiogenesismedicine.medical_treatmentOsteoimmunologyT cellPlasma CellsProgrammed Cell Death 1 ReceptorImmunologyOsteoclastsCell CommunicationReviewB7-H1 AntigenImmune tolerance03 medical and health sciencesImmune systemAntigens NeoplasmImmune ToleranceTumor MicroenvironmentmedicineAnimalsHumansImmunology and AllergyBone ResorptionImmunologic Surveillancebone marrow microenvironmentTumor microenvironmentbusiness.industryprogrammed cell death ligand 1Immunotherapymultiple myeloma030104 developmental biologymedicine.anatomical_structureprogrammed cell death 1osteoclastosteoblastCancer researchimmunotherapylcsh:RC581-607businessB7-H1 AntigenSignal TransductionFrontiers in Immunology
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Increased autophagy and apoptosis contribute to muscle atrophy in a myotonic dystrophy type 1 Drosophila model

2015

ABSTRACT Muscle mass wasting is one of the most debilitating symptoms of myotonic dystrophy type 1 (DM1) disease, ultimately leading to immobility, respiratory defects, dysarthria, dysphagia and death in advanced stages of the disease. In order to study the molecular mechanisms leading to the degenerative loss of adult muscle tissue in DM1, we generated an inducible Drosophila model of expanded CTG trinucleotide repeat toxicity that resembles an adult-onset form of the disease. Heat-shock induced expression of 480 CUG repeats in adult flies resulted in a reduction in the area of the indirect flight muscles. In these model flies, reduction of muscle area was concomitant with increased apopto…

lcsh:MedicineMedicine (miscellaneous)Genes InsectApoptosisDystrophyInhibitor of Apoptosis ProteinsAnimals Genetically ModifiedCTG repeat expansion0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsMyotonic DystrophyMyocyte0303 health sciencesTOR Serine-Threonine KinasesMyotonin-protein kinaseNuclear ProteinsMuscle atrophyUp-RegulationCell biologyMuscular AtrophyDrosophila melanogastermedicine.anatomical_structureFemalemedicine.symptomSignal TransductionResearch Articlelcsh:RB1-214congenital hereditary and neonatal diseases and abnormalitiesProgrammed cell deathNeuroscience (miscellaneous)BiologyMyotonic dystrophyMyotonin-Protein KinaseMuscleblindGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAutophagylcsh:PathologymedicineAnimalsHumans030304 developmental biologylcsh:RAutophagyDystrophySkeletal musclemedicine.diseaseMolecular biologyDisease Models AnimalMuscle atrophyTrinucleotide Repeat Expansion030217 neurology & neurosurgeryDisease Models & Mechanisms
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Apoptotic-like Leishmania exploit the host´s autophagy machinery to reduce T-cell-mediated parasite elimination

2015

Apoptosis is a well-defined cellular process in which a cell dies, characterized by cell shrinkage and DNA fragmentation. In parasites like Leishmania, the process of apoptosis-like cell death has been described. Moreover upon infection, the apoptotic-like population is essential for disease development, in part by silencing host phagocytes. Nevertheless, the exact mechanism of how apoptosis in unicellular organisms may support infectivity remains unclear. Therefore we investigated the fate of apoptotic-like Leishmania parasites in human host macrophages. Our data showed--in contrast to viable parasites--that apoptotic-like parasites enter an LC3(+), autophagy-like compartment. The compartm…

log.ph logarithmic phaseT-LymphocytesApoptosisMACS magnetic-associated cell sortingMacrophageMFI mean fluorescence intensityLeishmaniasisMOI multiplicity of infectionanti-inflammatoryLeishmaniaeducation.field_of_studyPhagocytesCFSE carboxyfluorescein succinimidyl esterTGFB transforming growth factorAcquired immune systemapoptotic-like LeishmaniaPS phosphatidylserinehuman primary macrophagesCell biologyβ; TT tetanus toxoidCorrigendumProgrammed cell deathautophagyPopulationAntigen presentationANXA5 annexin VBasic Science Research PapersBiologyPhagocytosisCM complete mediumMAP1LC3/LC3 microtubule-associated protein 1 light chain 3AnimalsHumansMHC major histocompatibility complexIF immunofluorescenceeducationMolecular Biologyimmune evasionPBMCs peripheral blood mononuclear cellsT-cell proliferationIntracellular parasiteMacrophagesstat.ph stationary phaseAutophagyLm LeishmaniaCell BiologyLeishmaniabiology.organism_classificationIL interleukinLAP LC3-associated phagocytosisLAPhMDM human monocyte derived macrophageAutophagy
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Intermittent ethanol exposure induces inflammatory brain damage and causes long-term behavioural alterations in adolescent rats

2007

Adolescent brain development seems to be important for the maturation of brain structures and behaviour. Intermittent binge ethanol drinking is common among adolescents, and this type of drinking can induce brain damage. Because we have demonstrated that chronic ethanol treatment induces inflammatory processes in the brain, we investigate whether intermittent ethanol intoxication enhances cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in adolescent rats, and whether these mediators induce brain damage and cause permanent cognitive dysfunctions. Adolescent rats were exposed to ethanol (3.0 g/kg) for two consecutive days at 48-h intervals over 14 days. Levels of COX-2, iN…

medicine.medical_specialtyCerebellumProgrammed cell deathIndomethacinHippocampusNitric Oxide Synthase Type IIInflammationBrain damageMotor ActivityNeuropsychological TestsDiscrimination Learningchemistry.chemical_compoundindomethacinInternal medicineintermittent ethanol intoxicationmedicineAnimalsDrug InteractionsRats WistarAnalysis of VarianceNeocortexEthanolbiologyBehavior AnimalCell DeathEthanolCaspase 3General NeuroscienceAnti-Inflammatory Agents Non-SteroidalBrainRecognition PsychologyRatsNitric oxide synthasemedicine.anatomical_structureEndocrinologychemistryAnimals NewbornneurobehaviourCyclooxygenase 2inflammationAnesthesiabiology.proteinEncephalitisadolescencemedicine.symptomPsychologyPsychomotor Performance
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Diagnosis, monitoring and management of immune-related adverse drug reactions of anti-PD-1 antibody therapy.

2015

PD-1 checkpoint inhibitors are associated with a specific spectrum of immune-related adverse events. This spectrum is different from toxicities known for kinase inhibitors or cytotoxic drugs. Since PD-1 directed therapies show effectivity in an increasing number of malignant diseases, their clinical usage will increase rapidly. Therefore clinicians from different specialities such as medical oncology, internal medicine, family doctors and emergency unit staff should be aware of the adverse effects of PD-1 checkpoint inhibitors to avoid delays in diagnosis and treatment. Based on pooled data from pivotal trials as reported by the European Medicines Agency, the present paper reviews incidence…

medicine.medical_specialtyDrug-Related Side Effects and Adverse Reactionsmedicine.medical_treatmentProgrammed Cell Death 1 ReceptorMedizinAntineoplastic AgentsPembrolizumabAntibodies Monoclonal HumanizedB7-H1 Antigen03 medical and health sciences0302 clinical medicineRefractoryMonitoring ImmunologicNeoplasmsmedicineEndocrine systemHumansRadiology Nuclear Medicine and imaging030212 general & internal medicineIntensive care medicineAdverse effectbusiness.industryAntibodies MonoclonalDisease ManagementGeneral MedicineImmunotherapymedicine.diseaseEarly DiagnosisNivolumabOncologyMethylprednisolone030220 oncology & carcinogenesisImmunologyNivolumabbusinessAdverse drug reactionImmunosuppressive Agentsmedicine.drugCancer treatment reviews
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Synergistic effects of fluticasone propionate and salmeterol on in vitro T-cell activation and apoptosis in asthma

2004

Background In asthma T cells are characterized by an increased activation state and by reduced apoptosis. Objective Because the clinical efficacy of inhaled corticosteroids combined with long-acting β 2 -agonists has been widely demonstrated in asthma, we studied, in vitro , the effect of fluticasone propionate (FP) and salmeterol alone and in combination on the activation and apoptosis of peripheral blood T cells (PBTs), on the expression of phosphorylated nuclear factor κB inhibitor (IκBα), and on the nuclear translocation of glucocorticoid receptor (GR) in PBTs from asthmatic subjects. Methods Apoptosis was evaluated on the basis of annexin V binding, whereas the expression of caspases 8…

medicine.medical_specialtyProgrammed cell deathAdolescentT cellT-LymphocytesImmunologyActive Transport Cell NucleusApoptosisAndrostadienes; Active Transport Cell Nucleus; NF-kappa B; Apoptosis; Humans; Albuterol; Receptors Glucocorticoid; Asthma; Child; Caspases; Lymphocyte Activation; Phosphorylation; I-kappa B Proteins; Adolescent; Drug Synergism; T-LymphocytesLymphocyte ActivationGlucocorticoid receptorReceptors GlucocorticoidNF-KappaB Inhibitor alphaAnnexinInternal medicinemedicineHumansImmunology and AllergyAlbuterolPhosphorylationChildSalmeterol XinafoateAndrostadieneChemistryActive Transport Cell NucleuNF-kappa BApoptosiDrug SynergismCaspaseAsthmaAndrostadienesIκBαEndocrinologymedicine.anatomical_structureApoptosisCaspasesFluticasoneI-kappa B ProteinI-kappa B ProteinsSalmeterolGlucocorticoidmedicine.drugHuman
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The Human Blastocyst Regulates Endometrial Epithelial Apoptosis in Embryonic Adhesion1

2000

The implanting blastocyst must appose and adhere to the endometrial epithelium and, subsequently, invade it. Locally regulated uterine epithelial apoptosis induced by the embryo is a crucial step of the epithelial invasion in rodents. To address the physiological relevance of this process in humans, we investigated the effect of single human blastocysts on the regulation of apoptosis in cultured human endometrial epithelial cells (hEEC) in both apposition and adhesion phases of implantation. Here, we report a co-ordinated embryonic regulation of hEEC apoptosis. In the apposition phase, the presence of a blastocyst rescues hEEC from the apoptotic pathway. However, when the human blastocyst a…

medicine.medical_specialtyProgrammed cell deathCell BiologyGeneral MedicineBiologyEmbryonic stem cellEpitheliumFas ligandCell biologyParacrine signallingEndocrinologymedicine.anatomical_structureReproductive MedicineApoptosisInternal medicinemedicineBlastocystCell adhesionBiology of Reproduction
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Midregion parathyroid hormone-related protein inhibits growth and invasion in vitro and tumorigenesis in vivo of human breast cancer cells.

2001

Parathyroid hormone-related protein (PTHrP) is critical for normal mammary development and is overexpressed by breast cancers. PTHrP is a peptide hormone that undergoes extensive post-translational processing, and PTHrP(38–94)-amide is one of the mature secretory forms of the peptide. In this study, we explored the effect of PTHrP(38–94)-amide in a panel of six breast cancer cell lines “in vitro” and in MDA-MB231 cells “in vivo” specifically examining cell viability, proliferation, invasiveness, and growth in nude mice. PTHrP(38–94)-amide markedly inhibited proliferation and also caused striking toxicity and accelerated cell death in breast cancer cells. In addition, direct injection of PTH…

medicine.medical_specialtyProgrammed cell deathEndocrinology Diabetes and MetabolismMammary glandMice NudeAntineoplastic AgentsBreast NeoplasmsCell CountBiologymedicine.disease_causeMiceInternal medicinemedicineTumor Cells CulturedAnimalsHumansOrthopedics and Sports MedicineNeoplasm Invasivenessskin and connective tissue diseasesParathyroid hormone-related proteinCell growthParathyroid Hormone-Related ProteinCancerProteinsNeoplasms Experimentalmedicine.diseasePeptide FragmentsDisease Models AnimalEndocrinologymedicine.anatomical_structureCell cultureCancer cellCancer researchFemaleCarcinogenesishormones hormone substitutes and hormone antagonistsCell DivisionJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
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Nitric oxide triggers mammary gland involution after weaning: remodelling is delayed but not impaired in mice lacking inducible nitric oxide synthase

2010

During mammary gland involution, different signals are required for apoptosis and tissue remodelling. To explore the role of NO in the involution of mammary tissue after lactation, NOS2 (inducible nitric oxide synthase)-KO (knockout) mice were used. No apparent differences were observed between NOS2-KO and WT (wild-type) animals during pregnancy and lactation. However, upon cessation of lactation, a notable delay in involution was observed, compared with WT mice. NOS2-KO mice showed increased phosphorylation of STAT (signal transducer and activator of transcription) 5 during weaning, concomitant with increased beta-casein mRNA levels when compared with weaned WT glands, both hallmarks of th…

medicine.medical_specialtyProgrammed cell deathNitric Oxide Synthase Type IIWeaningBiologyNitric OxideBiochemistryNitric oxideMicechemistry.chemical_compoundMammary Glands AnimalInternal medicinemedicineAnimalsInvolution (medicine)STAT3Molecular BiologyMammary gland involutionMice KnockoutCell BiologyAnimals SucklingProlactinMice Inbred C57BLNitric oxide synthaseEndocrinologychemistryApoptosisbiology.proteinSTAT proteinFemaleBiochemical Journal
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