Search results for "Programmed cell death"

showing 10 items of 609 documents

Analysis of BNIP3 and BNIP3L/Nix expression in cybrid cell lines harboring two LHON-associated mutations.

2019

Mitochondria are key players in cell death through the activation of the intrinsic apoptosis pathway. BNIP3 and BNIP3L/Nix are outer mitochondrial membrane bifunctional proteins which because of containing both BH3 and LIR domains play a role in cellular response to stress by regulation of apoptosis and selective autophagy. Leber’s Hereditary Optic Neuropathy (LHON) is the most common mitochondrial disease in adults, characterized by painless loss of vision caused by atrophy of the optic nerve. The disease in over 90% of cases is caused by one of three mutations in the mitochondrial genome: 11778G>A, 3460G>A or 14484T>C. The pathogenic processes leading to optic nerve degeneration …

AdultProgrammed cell deathMitochondrial diseaseApoptosisOptic Atrophy Hereditary LeberMitochondrionBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCell LineMitochondrial Proteins03 medical and health sciencesAtrophyProto-Oncogene ProteinsmedicineAutophagyHumans0303 health sciencesMutationTumor Suppressor Proteins030302 biochemistry & molecular biologyAutophagyIntrinsic apoptosisMembrane Proteinsmedicine.diseaseeye diseasesCell biologyApoptosisGenome MitochondrialMutationActa biochimica Polonica
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Cell Death and Oxidative Damage in Inflammatory Myopathies

1998

There is evidence that muscle fibers in denervating disorders and muscular dystrophies undergo apoptosis. In 21 patients with autoimmune inflammatory myopathies, we found no features of muscle fiber apoptosis such as DNA fragmentation or expression of apoptosis-related proteins. However, muscle fibers in myositis displayed distinct up-regulation of inducible and neuronal nitric oxide synthase (NOS). While inducible NOS was distinctly up-regulated on the sarcolemma of all kinds of muscle fibers neuronal NOS displayed increased expression in the sarcoplasm of damaged as well as atrophic muscle fibers. There were no disease-specific patterns in the different myositis subtypes. Enhanced express…

AdultProgrammed cell deathNecrosisAdolescentImmunologySarcoplasmNitric Oxide Synthase Type IIApoptosisNitric Oxide Synthase Type IDermatomyositisMyositis Inclusion BodyPathology and Forensic MedicineMiceReference ValuesMuscle fiber necrosismedicineAnimalsHumansImmunology and AllergyChildMuscle SkeletalMyositisAgedSarcolemmaCell DeathbiologyInfantDNAMiddle Agedmedicine.diseasePolymyositisCell biologyNitric oxide synthaseOxidative StressApoptosisChild PreschoolImmunologybiology.proteinRabbitsNitric Oxide Synthasemedicine.symptomClinical Immunology and Immunopathology
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Glutathione, oxidative stress and aging

1996

The free radical theory of aging proposes that the impairment in physiological performance associated with aging is caused by the detrimental effects of oxygen free radicals. This is interesting because it provides us with a theoretical framework to understand aging and because it suggests a rationale for intervention, i.e., antioxidant administration. Thus, the study of antioxidant systems of the cell may be very important in gerontological studies. Glutathione is one of the main nonprotein antioxidants in the cell which, together with its related enzymes, constitute the “glutathione system.” The involvement of glutathione in aging has been known since the early seventies. Several studies …

AgingProgrammed cell deathAntioxidantmedicine.medical_treatmentGeneral MedicineGlutathioneMitochondrionBiologyPharmacologyGPX4medicine.disease_causechemistry.chemical_compoundBiochemistrychemistryApoptosismedicineGeriatrics and GerontologyOxidative stressFree-radical theory of agingAGE
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Semi-Mechanistic Model for the Antitumor Response of a Combination Cocktail of Immuno-Modulators in Non-Inflamed (Cold) Tumors.

2021

Simple Summary The clinical efficacy of immunotherapies when treating cold tumors is still low, and different treatment combinations are needed when dealing with this challenging scenario. In this work, a middle-out strategy was followed to develop a model describing the antitumor efficacy of different immune-modulator combinations, including an antigen, a toll-like receptor-3 agonist, and an immune checkpoint inhibitor in mice treated with non-inflamed tumor cells. Our results support that clinical response requires antigen-presenting cell activation and also relies on the amount of CD8 T cells and tumor resistance mechanisms present. This mathematical model is a very useful platform to ev…

AgonistCancer ResearchProgrammed cell deathmedicine.drug_classmedicine.medical_treatmentcold tumorscombination of therapeuticsArticleAntigenmedicinepreclinicalDoubling timeimmuno-oncologyRC254-282biologybusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensImmunotherapydrug developmentmechanistic modelingOncologyDrug developmentCancer researchbiology.proteinAntibodybusinessCD8Cancers
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Induction of apoptosis by the adenosine derivative IB-MECA in parental or multidrug-resistant HL-60 leukemia cells: possible relationship to the effe…

2004

<i>Background:</i> The effects of the A<sub>3</sub> adenosine receptor (A<sub>3</sub>AR) agonist IB-MECA were examined in HL-60 leukemia and in its multidrug-resistant variant HL-60R cells. <i>Methods:</i> Cytotoxicity was evaluated by MTS assays and apoptosis by flow cytometry analyses of DNA fragmentation and phosphatidylserine exposure. The mRNAs of A<sub>3</sub>AR and inhibitor of apoptosis proteins (IAPs) were determined by RT-PCR. <i>Results:</i> A<sub>3</sub>AR expression was similar in HL-60 and HL-60R cells. At ≧100 µ<i>M</i>, IB-MECA exhibited strong cytotoxic and apoptotic effects in H…

AgonistProgrammed cell deathAdenosinemedicine.drug_classApoptosisHL-60 CellsBiologyInhibitor of apoptosisInhibitor of Apoptosis ProteinsDrug DiscoverymedicineNeoplasmHumansPharmacology (medical)PharmacologyGeneral Medicinemedicine.diseaseAdenosine A3 receptorFlow CytometryAdenosineDrug Resistance MultipleLeukemiaInfectious DiseasesOncologyBiochemistryApoptosisDrug Resistance NeoplasmA 3 adenosine receptor IB-MECA Apoptosis Multidrug resistance Inhibitor of apoptosis proteinsCancer researchmedicine.drugChemotherapy
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Induction of Apoptosis in Rat Cardiocytes by A3 Adenosine Receptor Activation and Its Suppression by Isoproterenol

2000

The purpose of the present study was to investigate the mechanisms involved in the induction of apoptosis in newborn cultured cardiomyocytes by activation of adenosine (ADO) A3 receptors and to examine the protective effects of beta-adrenoceptors. The selective agonist for A3 ADO receptors Cl-IB-MECA (2-chloro-N6-iodobenzyl-5-N-methylcarboxamidoadenosine) and the antagonist MRS1523 (5-propyl-2-ethyl-4-propyl-3-(ethylsulfanylcarbonyl)-6-phenylpy rid ine-5-carboxylate) were used. High concentrations of the Cl-IB-MECA (or = 10 microM) agonist induced morphological modifications of myogenic cells, such as rounding and retraction of cell body and dissolution of contractile filaments, followed by…

Agonistmedicine.medical_specialtyProgrammed cell deathAdenosineCardiotonic Agentsmedicine.drug_classApoptosisStimulationBiologyInternal medicinePurinergic P1 Receptor AgonistsmedicineAnimalsProtein kinase AReceptorCells CulturedMyocardiumReceptor Adenosine A3IsoproterenolReceptors Purinergic P1HeartCell BiologyAdenosineAdenosine receptorRatsCell biologyEndocrinologyApoptosisSignal Transductionmedicine.drugExperimental Cell Research
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Mitochondrial function in liver disease.

2006

Oxidative stress is involved in the pathogenesis and progression of different liver diseases, such as alcoholic liver disease and biliary cirrhosis. The increased mitochondrial production of O2(-) at complexes I and III, and consequently of H2O2 and other reactive oxygen species (ROS), triggered by NADH overproduction seems the major cause of mitochondrial and cellular oxidative stress and damage in chronic alcoholism. The mitochondrial oxidative stress renders hepatocytes susceptible to ethanol- or acetaldehyde-induced mitochondrial membrane permeability transition (MMPT) and apoptosis. Nitrosative stress contributes to cell death by peroxynitrite formation. The expression of the death rec…

Alcoholic liver diseaseProgrammed cell deathBiliary cirrhosisPopulationApoptosisMitochondria LiverMitochondrionmedicine.disease_causechemistry.chemical_compoundmedicineCardiolipinAnimalsHumanseducationLiver Diseases Alcoholicchemistry.chemical_classificationeducation.field_of_studyReactive oxygen speciesLiver Cirrhosis BiliaryLiver Diseasesmedicine.diseaseNADCell biologyRatsOxidative StresschemistryHepatocytesOxidative stressFrontiers in bioscience : a journal and virtual library
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Overexpression of genes involved in lymphocyte activation and regulation are associated with reduced CRM-derived cardiac remodelling after STEMI

2021

Abstract Aims Lymphopenia after ST-segment elevation myocardial infarction (STEMI) correlates with deleterious cardiac consequences and worse prognosis. An in-depth examination of genes implicated in lymphocyte proliferation, activation and regulation and their association with short- and long-term cardiac structure and function is therefore of great interest. Methods Peripheral blood mononuclear cells were isolated from 10 control subjects and 64 patients with a first STEMI treated with primary percutaneous coronary intervention and submitted to cardiac magnetic resonance after 1 week and 6 months. mRNA expression of genes implicated in lymphocyte activation (CD25 and CD69) and regulation …

Antigens Differentiation T-LymphocyteMale0301 basic medicinemedicine.medical_specialtyLymphocytemedicine.medical_treatmentProgrammed Cell Death 1 ReceptorImmunologyGene Expressionchemical and pharmacologic phenomenaLymphocyte proliferationLymphocyte Activation03 medical and health sciences0302 clinical medicineAntigens CDInternal medicineHumansImmunology and AllergyMedicineCytotoxic T cellCTLA-4 AntigenLectins C-TypeIL-2 receptorMyocardial infarctionGeneAgedPharmacologyVentricular Remodelingbusiness.industryInterleukin-2 Receptor alpha SubunitPercutaneous coronary interventionHearthemic and immune systemsOdds ratioMiddle Agedmedicine.diseaseMagnetic Resonance ImagingPathophysiology030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchLymphocyte activationLeukocytes MononuclearCardiologyST Elevation Myocardial InfarctionFemaleCardiology and Cardiovascular MedicinebusinessInternational Immunopharmacology
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Antitumoural Properties of Benzannelated Seven -Membered 5-fluorouracil Derivatives and Related Open Analogues. Molecular Markers for Apoptosis and C…

2005

Attention is increasingly being focussed on the cell cycle and apoptosis as potential targets for therapeutic intervention in cancer. We prepared a series of bioisosteric benzannelated seven-membered 5-FU O,N-acetals to test them against the MCF-7 human breast cancer cell line. Benzo-fused seven-membered O,O-acetals or their acyclic analogues led to the expected 5-FU O,N-acetals (or aminals), in addition to six- and 14-membered aminal structures and acyclic compounds. All the cyclic aminals provoked a G0/G1-phase cell cycle arrest, whereas Ftorafur, a known prodrug of 5-FU, and 1-[2-(2-hydroxymethyl-4-nitrophenoxy)-1-methoxyethyl]-5-fluorouracil (11) induced an S-phase cell cycle arrest. Al…

Antitumour drugs Breast cancer Cell cycle Programmed cell death Benzodioxepins
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Neuronal cell cycle: the neuron itself and its circumstances.

2015

Neurons are usually regarded as postmitotic cells that undergo apoptosis in response to cell cycle reactivation. Nevertheless, recent evidence indicates the existence of a defined developmental program that induces DNA replication in specific populations of neurons, which remain in a tetraploid state for the rest of their adult life. Similarly, de novo neuronal tetraploidization has also been described in the adult brain as an early hallmark of neurodegeneration. The aim of this review is to integrate these recent developments in the context of cell cycle regulation and apoptotic cell death in neurons. We conclude that a variety of mechanisms exists in neuronal cells for G1/S and G2/M check…

ApoptosisBrdU 5-bromo-2′-deoxyuridineReviewp75NTR neurotrophin receptor p75Nervous SystemG0 quiescent stateCKI Cdk-inhibitorNeuronsCell DeathNeurodegenerationCell CycleapoptosisNeurodegenerative DiseasesCell cycleCell biologymedicine.anatomical_structureInk inhibitor of kinaseBDNF brain-derived neurotrophic factorp38MAPK p38 mitogen-activated protein kinaseG2 growth phase 2Programmed cell deathS-phasePD Parkinson diseaseRb RetinoblastomaMcm2 minichromosome maintenance 2PCNA proliferating cell nuclear antigenMitosisContext (language use)BiologyCdk cyclin-dependent kinaseCNS central nervous systemS-phase synthesis phase.Cip/Kip cyclin inhibitor protein/kinase inhibitor proteinmedicineAnimalsHumansMolecular BiologyMitosisTetraploidAD Alzheimer diseasecell cycle re-entryDNA replicationCell BiologyNeuronmedicine.diseaseG1 growth phase 1neuronRGCs retinal ganglion cellsCell cycle re-entrytetraploidnervous systemApoptosisNeuronDevelopmental BiologyCell cycle (Georgetown, Tex.)
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