Search results for "Apoptosis."

showing 10 items of 1794 documents

Role of persistent CMV infection in configuring T cell immunity in the elderly

2007

Abstract Ageing is associated with declines in many physiological parameters, including multiple immune system functions. The rate of acceleration of the frequency of death due to cardiovascular disease or cancer seems to increase with age from middle age up to around 80 years, plateauing thereafter. Mortality due to infectious disease, however, does not plateau, but continues to accelerate indefinitely. The elderly commonly possess oligoclonal expansions of T cells, especially of CD8 cells, which, surprisingly, are often associated with cytomegalovirus (CMV) seropositivity. This in turn is associated with many of the same phenotypic and functional alterations to T cell immunity that have b…

lcsh:Immunologic diseases. AllergyAgingbiologybusiness.industryImmunologyMembrane raftReviewDiseaseImmunosenescencelcsh:GeriatricsBioinformaticsVaccinationlcsh:RC952-954.6aged aging antigen expression apoptosis cancer incidence CD4+ T lymphocyte CD8+ T lymphocyte cellular immunityAgeingImmune systemInfectious disease (medical specialty)ImmunityImmunologybiology.proteinMedicineAntibodybusinesslcsh:RC581-607Immunity & Ageing
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The NG2 Proteoglycan Protects Oligodendrocyte Precursor Cells against Oxidative Stress via Interaction with OMI/HtrA2.

2015

The NG2 proteoglycan is characteristically expressed by oligodendrocyte progenitor cells (OPC) and also by aggressive brain tumours highly resistant to chemo- and radiation therapy. Oligodendrocyte-lineage cells are particularly sensitive to stress resulting in cell death in white matter after hypoxic or ischemic insults of premature infants and destruction of OPC in some types of Multiple Sclerosis lesions. Here we show that the NG2 proteoglycan binds OMI/HtrA2, a mitochondrial serine protease which is released from damaged mitochondria into the cytosol in response to stress. In the cytosol, OMI/HtrA2 initiates apoptosis by proteolytic degradation of anti-apoptotic factors. OPC in which NG…

lcsh:MedicineApoptosisdrug effects [Cytosol]HTRA2 protein humangenetics [RNA Small Interfering]genetics [Serine Endopeptidases]genetics [Glioblastoma]570 Life sciencespathology [Glioblastoma]MiceCytosolCerebellumpathology [Cerebellum]RNA Small Interferinglcsh:Sciencemetabolism [Antigens]Mice Knockoutchondroitin sulfate proteoglycan 4metabolism [Proteoglycans]Brain NeoplasmsSerine Endopeptidasesdrug effects [Mitochondria]metabolism [Cerebellum]High-Temperature Requirement A Serine Peptidase 2Mitochondriametabolism [Brain Neoplasms]Gene Expression Regulation Neoplasticpharmacology [Antibodies Neutralizing]genetics [Mitochondrial Proteins]Proteoglycans570 BiowissenschaftenResearch ArticleProtein BindingSignal Transductionpathology [Brain Neoplasms]Primary Cell Culturedrug effects [Cerebellum]drug effects [Apoptosis]metabolism [Mitochondrial Proteins]Mitochondrial Proteinsantagonists & inhibitors [Proteoglycans]pharmacology [Hydrogen Peroxide]genetics [Antigens]Cell Line Tumormetabolism [Serine Endopeptidases]AnimalsHumansddc:610metabolism [RNA Small Interfering]Antigenslcsh:RHtra2 protein mouseHydrogen Peroxidemetabolism [Mitochondria]Antibodies Neutralizinggenetics [Proteoglycans]genetics [Brain Neoplasms]Mice Inbred C57BLOxidative Stressnervous systemlcsh:Qmetabolism [Cytosol]Glioblastomametabolism [Glioblastoma]
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Progenitor death drives retinal dysplasia and neuronal degeneration in a mouse model of Atrip-Seckel syndrome

2020

ABSTRACT Seckel syndrome is a type of microcephalic primordial dwarfism (MPD) that is characterized by growth retardation and neurodevelopmental defects, including reports of retinopathy. Mutations in key mediators of the replication stress response, the mutually dependent partners ATR and ATRIP, are among the known causes of Seckel syndrome. However, it remains unclear how their deficiency disrupts the development and function of the central nervous system (CNS). Here, we investigated the cellular and molecular consequences of ATRIP deficiency in different cell populations of the developing murine neural retina. We discovered that conditional inactivation of Atrip in photoreceptor neurons …

lcsh:MedicineMedicine (miscellaneous)315BlindnessMicechemistry.chemical_compoundImmunology and Microbiology (miscellaneous)Cell DeathneurodevelopmentStem CellsNeurodegenerationapoptosisneurodegenerationSyndromeCell biologyDNA-Binding Proteinsdna damage responsemedicine.anatomical_structurePhotoreceptor Cells VertebrateResearch Articlelcsh:RB1-214NeurogenesisNeuroscience (miscellaneous)Embryonic DevelopmentBiologyRetinaGeneral Biochemistry Genetics and Molecular Biologylcsh:PathologymedicineAnimalsAbnormalities MultipleProgenitor cellVision OcularAdaptor Proteins Signal TransducingCell ProliferationProgenitorRetinalcsh:RRetinalEmbryo Mammalianmedicine.diseasephotoreceptorDisease Models AnimalSeckel syndromechemistryvisual system developmentNerve DegenerationRetinal dysplasiaRetinal DysplasiaTumor Suppressor Protein p53Primordial dwarfismDNA DamageDisease Models & Mechanisms
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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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In Vitro Modulation of P-Glycoprotein Activity by Euphorbia intisy Essential Oil on Acute Myeloid Leukemia Cell Line HL-60R

2021

Euphorbia species have a large spectrum of traditional medicinal uses. We tested the biological activities of the essential oil (EO) of Euphorbia intisy Drake in an acquired multidrug resistance leukemia model to assess whether the EO obtained by hydrodistillation of stems was able to reverse the resistant phenotype. HL-60R cell lines are characterized by the overexpression of P-glycoprotein (P-gp), inhibitors of apoptosis proteins (IAPs) and constitutive expression of NF-κB. EO chemical composition was determined by GC/MS analysis

lcsh:Medicinelcsh:RS1-441Pharmaceutical ScienceP-glycoprotein01 natural sciencesessential oilNF-κBFlow cytometrylcsh:Pharmacy and materia medicamultidrug resistanceDrug DiscoverymedicineChemosensitizing agentSettore BIO/15 - Biologia FarmaceuticaP-glycoproteincancer cellbiologymedicine.diagnostic_test010405 organic chemistryChemistrylcsh:RMyeloid leukemiamyeloid leukemia cellSettore CHIM/08 - Chimica FarmaceuticaMolecular biologyIn vitro0104 chemical sciencesMultiple drug resistance010404 medicinal & biomolecular chemistryApoptosisCell cultureSettore BIO/03 - Botanica Ambientale E ApplicataSettore BIO/14 - Farmacologiabiology.proteinMolecular Medicineinhibitors of apoptosis proteinsPharmaceuticals
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Anti-tumor activity of the methanolic extracts of Salvia menthifolia

2012

In the present research we investigated the anti-proliferative activity of Salvia menthifolia Ten. (formerly Salvia menthaefolia), Lamiaceae, on a glioblastoma cell line, since up to date poor therapeutic results have been reported for treatment of malignant glioblastoma. Methanol extracts from different anatomical parts of S. menthifolia were tested on DBTRG-05MG cell line by MTT assay. The most active primary stems extract was also evaluated for apoptosis induction. Results confirmed the anti-tumor property of all the organs and demonstrated that the primary stems extract induced apoptosis after 4 h with the highest values of DNA fragmentation after 6 to 24 h. Some extracts were also HPLC…

lcsh:RS1-441Salvialcsh:Pharmacy and materia medicachemistry.chemical_compoundapoptosis glioblastoma Salvia menthifolia sageCaffeic acidMTT assaySettore BIO/15 - Biologia FarmaceuticaGeneral Pharmacology Toxicology and Pharmaceuticsapoptosis; glioblastoma; Salvia menthifolia; sageapoptosis glioblastomabiologyTraditional medicineRosmarinic acidapoptosisglioblastomaSalvia menthifoliabiology.organism_classificationQuercitrinSettore CHIM/08 - Chimica FarmaceuticasagechemistryBiochemistryPolyphenolSettore BIO/03 - Botanica Ambientale E ApplicataDNA fragmentationLamiaceae
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Toxicity of Branched-Chain Fatty Acids in Conjunctival Cell Line

2007

International audience; Purpose:: Tear film lipid composition is modified in patients suffering from chronic blepharitis. We previously found that branched chain fatty acids (BCFA) were significantly increased in tears of these patients, suggesting that BCFA may be involved in the disease. The toxicity of different BCFA as potent inducers of apoptosis has already been established in various cell lines but not in the conjunctiva. The aim of this work was to assess the toxic effects of BCFA in cultures of Chang conjunctival cells. Methods:: Chang’s human conjunctival cells were cultured during 4 or 24h with various concentrations of IsoC16 and IsoC20 as BCFA (from 50 to 200µM), by comparison …

lipids[SDV] Life Sciences [q-bio]conjunctivacell death[SPI.GPROC] Engineering Sciences [physics]/Chemical and Process Engineering[SDV]Life Sciences [q-bio][SDV.IDA]Life Sciences [q-bio]/Food engineeringapoptosis[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process Engineering[SDV.IDA] Life Sciences [q-bio]/Food engineering
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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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A minireview on NHE1 inhibitors. A rediscovered hope in oncohematology.

2015

Background: Na+/H+ exchanger-1 (NHE-1) is involved in pH regulation and is up-regulated in different malignancies. Activation of NHE-1 is one way for allowing cells to avoid intracellular acidification and protect them against apoptosis. Inhibitors of NHE-1 are able to decrease intracellular pH and induce apoptosis. Some statins can also act by partial inhibition of NHE-1. This review presents progress in understanding the mechanisms of action of these inhibitors, connections with certain genetic mutations and acquired treatment resistance, as well as new patents on them. Methods: A MEDLINE search for original and review articles using key terms, Na+/H+ exchanger, leukemia, cariporide, and …

lovastatinlcsh:MedicineApoptosisPharmacologyGuanidinesAmiloridep-glycoproteinhemic and lymphatic diseasesDrug InteractionsSulfonesCation Transport ProteinsSodium-Hydrogen Exchanger 1leukemiaMyeloid leukemiaHydrogen-Ion ConcentrationSorafenibUp-RegulationLeukemiaLeukemia Myeloid AcuteImatinib MesylateSignal transductionTyrosine kinasemedicine.drugSignal TransductionSorafenibNiacinamideisoprenylationSodium-Hydrogen Exchangersbcr/ablAntineoplastic AgentsGenes ablGeneral Biochemistry Genetics and Molecular BiologystatinsPatents as TopicCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansProtein Kinase Inhibitorscariporidena+/h+ exchangerTumor hypoxiabusiness.industryPhenylurea Compoundslcsh:ROsmolar Concentrationintracellular phmedicine.diseaseImatinib mesylatefms-Like Tyrosine Kinase 3Fms-Like Tyrosine Kinase 3MutationCancer researchTumor Hypoxiaflt3/itdHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessHeme Oxygenase-1DNA DamageBiomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
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Mutant HRAS as novel target for MEK and mTOR inhibitors.

2015

HRAS is a frequently mutated oncogene in cancer. However, mutant HRAS as drug target has not been investigated so far. Here, we show that mutant HRAS hyperactivates the RAS and the mTOR pathway in various cancer cell lines including lung, bladder and esophageal cancer. HRAS mutation sensitized toward growth inhibition by the MEK inhibitors AZD6244, MEK162 and PD0325901. Further, we found that MEK inhibitors induce apoptosis in mutant HRAS cell lines but not in cell lines lacking RAS mutations. In addition, knockdown of HRAS by siRNA blocked cell growth in mutant HRAS cell lines. Inhibition of the PI3K pathway alone or in combination with MEK inhibitors did not alter signaling nor had an imp…

mTOR inhibitorMutantBlotting Western610 Medicine & healthApoptosisMice SCIDCell LineProto-Oncogene Proteins p21(ras)chemistry.chemical_compoundCell Line TumorNeoplasmsMedicineAnimalsHumansHRASHRAS mutationsProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationGeneticsMitogen-Activated Protein Kinase KinasesMEK inhibitorOncogeneCell growthbusiness.industryMEK inhibitorTOR Serine-Threonine KinasesDiphenylamineXenograft Model Antitumor AssaysTumor Burdenlung cancer10219 Clinic for Gastroenterology and HepatologyCell Transformation NeoplasticOncologychemistry10032 Clinic for Oncology and HematologyBenzamidesMutationCancer researchbladder cancer2730 OncologyBenzimidazolesRNA InterferenceSignal transductionGrowth inhibitionbusinessSignal TransductionResearch PaperOncotarget
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