Search results for " cell death"

showing 10 items of 646 documents

Ca2+ signalling plays a role in celastrol‐mediated suppression of synovial fibroblasts of rheumatoid arthritis patients and experimental arthritis in…

2019

Background and purpose Celastrol exhibits anti-arthritic effects in rheumatoid arthritis (RA), but the role of celastrol-mediated Ca2+ mobilization in treatment of RA remains undefined. Here, we describe a regulatory role for celastrol-induced Ca2+ signalling in synovial fibroblasts of RA patients and adjuvant-induced arthritis (AIA) in rats. Experimental approach We used computational docking, Ca2+ dynamics and functional assays to study the sarcoplasmic/endoplasmic reticulum Ca2+ ATPase pump (SERCA). In rheumatoid arthritis synovial fibroblasts (RASFs)/rheumatoid arthritis fibroblast-like synoviocytes (RAFLS), mechanisms of Ca2+ -mediated autophagy were analysed by histological, immunohis…

0301 basic medicinemusculoskeletal diseasesMaleProgrammed cell deathSERCAArthritisSarcoplasmic Reticulum Calcium-Transporting ATPasesArthritis RheumatoidRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBAPTAmedicineAutophagyAnimalsHumansCalcium SignalingCells CulturedPharmacologyMice KnockoutGene knockdownbiologyChemistrySynovial MembraneCalpainFibroblastsmedicine.diseaseResearch PapersArthritis ExperimentalTriterpenesCalcineurin030104 developmental biologyGene Expression RegulationCelastrolbiology.proteinCancer researchPentacyclic Triterpenes030217 neurology & neurosurgeryResearch PaperBritish Journal of Pharmacology
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Wip1 phosphatase: between p53 and MAPK kinases pathways.

2016

IF 5.008; International audience; Cells undergoing oncogenic transformation frequently inactivate tumor suppressor pathways that could prevent their uncontrolled growth. Among those pathways p53 and p38MAPK pathways play a critical role in regulation of cell cycle, senescence and cell death in response to activation of oncogenes, stress and DNA damage. Consequently, these two pathways are important in determining the sensitivity of tumor cells to anti-cancer treatment. Wild type p53-induced phosphatase, Wip1, is involved in governance of both pathways. Recently, strategies directed to manipulation with Wip1 activity proposed to advance current day anticancer treatment and novel chemical com…

0301 basic medicinep53Programmed cell deathDNA damagetumor suppressorPhosphatase[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyReviewPyruvate dehydrogenase phosphataseBiologyBioinformaticsmedicine.disease_causechemotherapyp38 Mitogen-Activated Protein Kinases[ SDV.CAN ] Life Sciences [q-bio]/Cancerphosphatase03 medical and health sciencesmedicineAnimalsHumansGenetically modified animal[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyCell CycleCell cycleCell biologyProtein Phosphatase 2C030104 developmental biologyCell Transformation NeoplasticOncologyMutationSignal transductionTumor Suppressor Protein p53CarcinogenesisDNA DamageSignal TransductionOncotarget
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Antiviral Properties of Chemical Inhibitors of Cellular Anti-Apoptotic Bcl-2 Proteins

2017

Viral diseases remain serious threats to public health because of the shortage of effective means of control. To combat the surge of viral diseases, new treatments are urgently needed. Here we show that small-molecules, which inhibit cellular anti-apoptotic Bcl-2 proteins (Bcl-2i), induced the premature death of cells infected with different RNA or DNA viruses, whereas, at the same concentrations, no toxicity was observed in mock-infected cells. Moreover, these compounds limited viral replication and spread. Surprisingly, Bcl-2i also induced the premature apoptosis of cells transfected with viral RNA or plasmid DNA but not of mock-transfected cells. These results suggest that Bcl-2i sensiti…

0301 basic medicinevirusesFAMILY INHIBITORSlcsh:QR1-502Virus Replicationlcsh:Microbiologychemistry.chemical_compoundTranscription (biology)SALIPHENYLHALAMIDEhost responseTRANSCRIPTIONprogrammed cell deathinnate immunity1183 Plant biology microbiology virologySulfonamidesAniline CompoundsapoptosisTransfection3. Good healthInfectious DiseasesProto-Oncogene Proteins c-bcl-2X-L INHIBITORVirus DiseasesvirustauditVirusesRNA ViralBiologyTransfectionta3111Antiviral AgentsArticleCell LineMicrobiology in the medical areaantiviral agent03 medical and health sciencesohjelmoitunut solukuolemaVirologyMikrobiologi inom det medicinska områdetHumansMetabolomicsBenzothiazolesInnate immune systemapoptosis; antiviral agent; innate immunity; host responseZIKA VIRUS-INFECTIONCHRONIC LYMPHOCYTIC-LEUKEMIAPOTENTta1183INFLUENZA-Ata1182RNAIsoquinolinesVirology030104 developmental biologyViral replicationchemistryCell cultureApoptosisCELLSREPLICATIONDNA Viral3111 BiomedicineDNA
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Surviving the heat: heterogeneity of response inSaccharomyces cerevisiaeprovides insight into thermal damage to the membrane

2015

Environmental heat stress impacts on the physiology and viability of microbial cells with concomitant implications for microbial activity and diversity. Previously, it has been demonstrated that gradual heating of Saccharomyces cerevisiae induces a degree of thermal resistance, whereas a heat shock results in a high level of cell death. Here, we show that the impact of exogenous nutrients on acquisition of thermal resistance differs between strains. Using single-cell methods, we demonstrate the extent of heterogeneity of the heat-stress response within populations of yeast cells and the presence of subpopulations that are reversibly damaged by heat stress. Such cells represent potential for…

0303 health sciencesProgrammed cell deathmedicine.diagnostic_testbiology030306 microbiologyEcologyThermal resistanceCellSaccharomyces cerevisiaeHomeoviscous adaptationbiology.organism_classification7. Clean energyMicrobiologyYeastFlow cytometryCell biology03 medical and health sciencesmedicine.anatomical_structure13. Climate actionmedicineAdaptationEcology Evolution Behavior and Systematics030304 developmental biologyEnvironmental Microbiology
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CD73-generated extracellular adenosine in chronic lymphocytic leukemia creates local conditions counteracting drug-induced cell death

2011

Abstract Extracellular adenosine (ADO), generated from ATP or ADP through the concerted action of the ectoenzymes CD39 and CD73, elicits autocrine and paracrine effects mediated by type 1 purinergic receptors. We have tested whether the expression of CD39 and CD73 by chronic lymphocytic leukemia (CLL) cells activates an adenosinergic axis affecting growth and survival. By immunohistochemistry, CD39 is widely expressed in CLL lymph nodes, whereas CD73 is restricted to proliferation centers. CD73 expression is highest on Ki-67+ CLL cells, adjacent to T lymphocytes, and is further localized to perivascular areas. CD39+/CD73+ CLL cells generate ADO from ADP in a time- and concentration-dependen…

AdenosineCellular differentiationChronic lymphocytic leukemia5'-Nucleotidase; Adenosine; Adenosine Diphosphate; Adenosine Triphosphate; Antigens CD; Antineoplastic Agents Phytogenic; Apyrase; Autocrine Communication; Cell Death; Cell Differentiation; Cell Movement; Cell Survival; Etoposide; Extracellular Space; GPI-Linked Proteins; Humans; Leukemia Lymphocytic Chronic B-Cell; Paracrine Communication; Receptor Adenosine A2A; Tumor Cells Cultured; Biochemistry; Immunology; Hematology; Cell BiologyMICROENVIRONMENTCD38BiochemistryACTIVATIONAdenosine TriphosphateCell MovementPhytogenichemic and lymphatic diseasesTumor Cells CulturedChronic5'-NucleotidaseEtoposideLeukemiaCulturedCell DeathTUMOR-GROWTHApyrasePurinergic receptorCell DifferentiationHematologyLymphocyticCDTumor CellsCell biologyAdenosine DiphosphateAutocrine CommunicationLeukemiaReceptorIMMUNE SUPPRESSIONReceptor Adenosine A2ACell SurvivalImmunologyAntineoplastic AgentsAdenosinergicBiologyGPI-Linked ProteinsDAMAGE-INDUCED APOPTOSISAdenosine A2AParacrine signallingAntigens CDParacrine CommunicationmedicineHumansAntigensAutocrine signallingImmunobiologyB-CellCell BiologyDAMAGE-INDUCED APOPTOSIS; T-CELLS; IMMUNE SUPPRESSION; ZAP-70 EXPRESSION; TUMOR-GROWTH; RECEPTOR; CD73; ACTIVATION; CD38; MICROENVIRONMENTmedicine.diseaseAntineoplastic Agents PhytogenicLeukemia Lymphocytic Chronic B-CellSettore MED/15 - MALATTIE DEL SANGUET-CELLSCD73Extracellular SpaceZAP-70 EXPRESSIONCD38Blood
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Contribution of IL-17-producing {gamma}{delta} T cells to the efficacy of anticancer chemotherapy.

2011

IL-17 production by γδ T cells is required for tumor cell infiltration by IFN-γ–producing CD8+ T cells and inhibition of tumor growth in response to anthracyclines.

Adoptive cell transferMESH : AgedMESH : Equipment DesignCD8-Positive T-LymphocytesMESH: CatheterizationInterleukin-23MESH: Long-Term CareMice0302 clinical medicineMESH : CatheterizationT-Lymphocyte SubsetsMESH: NursingImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyInterferon gammaMESH: Quality of Health CareMESH: Professional Review OrganizationsMESH: AgedMESH : Gels0303 health sciencesMice Inbred BALB CCell DeathInterleukin-17MESH : Methylene BlueMESH : Quality of Health CareReceptors Antigen T-Cell gamma-deltaChemotherapy regimenMESH: Transplantation Autologous3. Good healthMESH: Cosmetic TechniquesTreatment Outcomemedicine.anatomical_structureMESH : Cadaver[SDV.IMM]Life Sciences [q-bio]/ImmunologyImmunogenic cell deathSarcoma ExperimentalInterleukin 17MESH : DissectionMESH : Long-Term CareMESH: Nursing CareMESH: Adipose Tissuemedicine.drugSignal TransductionMESH : Transplantation Autologous[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Feasibility StudiesMESH: GelsT cellMESH : MaleImmunologyMESH: DissectionAntineoplastic AgentsBiologyMESH : NursingMESH : Adipose TissueArticleMESH : Facial Muscles03 medical and health sciencesInterferon-gammaLymphocytes Tumor-InfiltratingImmune systemAntigenCell Line TumorMESH: Patient Care PlanningmedicineMESH: CadaverAnimalsMESH : Patient Care Planning030304 developmental biologyMESH: Humansbusiness.industryMESH: Facial MusclesT-cell receptorMESH : HumansCorrectionMESH: MaleMice Inbred C57BLMESH : Cosmetic TechniquesDoxorubicinImmunologyCancer researchMESH : Nursing CareMESH : Professional Review OrganizationsbusinessMESH: Feasibility StudiesCD8030215 immunologyMESH: Methylene BlueMESH: Equipment Design
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Lymphoma cell apoptosis in the liver induced by distant murine cytomegalovirus infection.

2006

ABSTRACTCytomegalovirus (CMV) poses a threat to the therapy of hematopoietic malignancies by hematopoietic stem cell transplantation, but efficient reconstitution of antiviral immunity prevents CMV organ disease. Tumor relapse originating from a minimal residual leukemia poses another threat. Although a combination of risk factors was supposed to enhance the incidence and severity of transplantation-associated disease, a murine model of a liver-adapted B-cell lymphoma has previously shown a survival benefit and tumor growth inhibition by nonlethal subcutaneous infection with murine CMV. Here we have investigated the underlying antitumoral mechanism. Virus replication proved to be required, …

Adoptive cell transferProgrammed cell deathMuromegalovirusLymphoma B-CellCD30Lymphomamedicine.medical_treatmentImmunologyApoptosisHematopoietic stem cell transplantationBiologyCD8-Positive T-Lymphocytesmedicine.disease_causeLymphoma T-CellMicrobiologyVirusHerpesviridaeMiceVirologyCell Line TumormedicineAnimalsPoint MutationBone Marrow TransplantationMice Inbred BALB CHerpesviridae Infectionsmedicine.diseaseVirologyAdoptive TransferLymphomaLeukemiaLiverMice Inbred DBAInsect ScienceNIH 3T3 CellsPathogenesis and ImmunityFemaleJournal of virology
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Low bcl-2 expression and increased spontaneous apoptosis in T-lymphocytes from newly-diagnosed IDDM patients.

1995

The bcl-2 gene product has been shown to regulate apoptotic cell death, and its dysregulation has been shown to induce several abnormalities in the immune system. No data exist regarding bcl-2 expression in autoimmune diseases, such as human insulin-dependent diabetes mellitus (IDDM). We investigated bcl-2 protein expression by testing T lymphocytes from 15 newly-diagnosed (3 weeks) IDDM patients in comparison to 10 age-matched control subjects. The expression of bcl-2 on CD3+ lymphocyte subsets was investigated after membrane permeabilization by two- or three-colour immunofluorescence. When the percentage and mean fluorescence intensity (MFI) of bcl-2+/CD3+ cells from normal individuals an…

AdultBlood GlucoseMaleProgrammed cell deathmedicine.medical_specialtyAdolescentCD3 ComplexEndocrinology Diabetes and MetabolismLymphocyteCD3T-LymphocytesGene ExpressionApoptosisBiologychemistry.chemical_compoundImmune systemAntigens CDReference ValuesRisk FactorsT-Lymphocyte SubsetsInternal medicineProto-Oncogene ProteinsInternal MedicinemedicineHumansFamilyPropidium iodideAutoantibodiesAutoimmune diseaseGlycated HemoglobinT lymphocytemedicine.diseaseFlow Cytometrymedicine.anatomical_structureEndocrinologyDiabetes Mellitus Type 1chemistryProto-Oncogene Proteins c-bcl-2ApoptosisCase-Control Studiesbiology.proteinFemaleDiabetologia
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CD4+ CCR5+ and CD4+ CCR3+ lymphocyte subset and monocyte apoptosis in patients with acute visceral leishmaniasis

2004

The potential involvement of apoptosis in the pathogenesis of visceral leishmaniasis (VL) was examined by studying spontaneous and Leishmania antigen (LAg)-induced apoptosis using cryopreserved peripheral blood mononuclear cells (PBMC) of Sicilian patients with VL. Results indicate that monocytes and T lymphocytes from acute VL patients show a significantly higher level of apoptosis compared with that observed in healed subjects. The percentage of apoptotic cells was higher in monocytes than in T lymphocytes. T cells involved in programmed cell death (PCD) were mainly of the CD4(+) phenotype. In particular, the T helper 1-type (Th1) subset, as evaluated by chemokine receptor-5 (CCR5) expres…

AdultCD4-Positive T-LymphocytesProgrammed cell deathChemokineReceptors CCR5Receptors CCR3ImmunologyAntigens ProtozoanApoptosisCD8-Positive T-LymphocytesBiologyPeripheral blood mononuclear cellMonocytesParacrine signallingAntigenmedicineHumansImmunology and Allergyfas ReceptorAutocrine signallingCells CulturedMonocyteOriginal ArticlesTh1 CellsLymphocyte Subsetsmedicine.anatomical_structureApoptosisAcute DiseaseImmunologyLeukocytes Mononuclearbiology.proteinLeishmaniasis VisceralReceptors ChemokineImmunology
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Impact of a preceding radiotherapy on the outcome of immune checkpoint inhibition in metastatic melanoma: a multicenter retrospective cohort study of…

2020

BackgroundImmune checkpoint inhibition (ICI) is an essential treatment option in melanoma. Its outcome may be improved by a preceding radiation of metastases. This study aimed to investigate the impact of a preceding radiotherapy on the clinical outcome of ICI treatment.MethodsThis multicenter retrospective cohort study included patients who received anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) or anti-programmed cell death protein 1 (PD-1) ICI with or without preceding radiotherapy for unresectable metastatic melanoma. ICI therapy outcome was measured as best overall response (BOR), progression-free (PFS) and overall survival (OS). Response and survival analyses were adjusted …

AdultMale0301 basic medicineOncologyCancer Researchmedicine.medical_specialtySkin NeoplasmsMetastatic melanoma2435medicine.medical_treatmentProgrammed Cell Death 1 ReceptorImmunologyMedizin03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansImmunology and AllergyCTLA-4 Antigen1506Immune Checkpoint InhibitorsMelanomaradiotherapyRC254-282Survival analysisRetrospective StudiesClinical/Translational Cancer ImmunotherapyPharmacologybusiness.industryMelanomaConfoundingNeoplasms. Tumors. Oncology. Including cancer and carcinogensRetrospective cohort studyChemoradiotherapyMiddle Agedmedicine.diseaseProgression-Free SurvivalImmune checkpointRadiation therapy030104 developmental biologyOncology030220 oncology & carcinogenesisRelative riskMolecular MedicineFemalebusinessJournal for ImmunoTherapy of Cancer
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