Search results for "Programmed cell death"

showing 10 items of 609 documents

Abstract 4219: Lysosomal membrane permeabilization, a novel anticancer mechanism induced by pterostilbene

2011

Abstract Pterostilbene (Pter) (3,5-dimethoxy-4′-hydroxystilbene), a natural dimethylated analog of resveratrol, is a phytoalexin abundant in plants and fruits with a number of potential benefits for human health. Darakchasava, an Indian herbal preparation of Vitis Vinifera, contains Pter and is prescribed as a cardiotonic in ayurvedic and traditional medicine. Furthermore, some observations indicate that Pter can be beneficial in the prevention and treatment of different diseases such as diabetes, dyslipidemia, or cancer. Pter shows higher bioavailability than resveratrol. The substitution of two OH groups (positions 3 and 5) by methyl groups increases the stabilityof the molecule and its r…

CathepsinCancer ResearchProgrammed cell deathPterostilbenebiologyCaspase 3ResveratrolMolecular biologychemistry.chemical_compoundLysosomal lumenOncologyBiochemistrychemistryApoptosisbiology.proteinCaspaseCancer Research
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Characteristic ERK1/2 signaling dynamics distinguishes necroptosis from apoptosis

2021

International audience; ERK1/2 involvement in cell death remains unclear, although many studies have demonstrated the importance of ERK1/2 dynamics in determining cellular re- sponses. To untangle how ERK1/2 contributes to two cell death programs, we investigated ERK1/2 signaling dynamics during hFasL-induced apoptosis and TNF-induced necroptosis in L929 cells. We observed that ERK1/2 inhibition sensi- tizes cells to apoptosis while delaying necroptosis. By monitoring ERK1/2 activity by live-cell imaging using an improved ERK1/2 biosensor (EKAR4.0), we reported differential ERK1/2 signaling dynamics between cell survival, apoptosis, and nec- roptosis. We also decrypted a temporally shifted …

Cell biologyProgrammed cell deathScience[SDV]Life Sciences [q-bio]Necroptosis[SDV.BBM.BP] Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsPROTEINMECHANISMSESCRTACTIVATION03 medical and health sciences0302 clinical medicineINFLAMMATIONGene expressionMedicine and Health SciencesKINASEBiology030304 developmental biology0303 health sciencesMultidisciplinaryIDENTIFICATIONChemistryNECROSISQDynamics (mechanics)Biology and Life SciencesErk1 2 signalingCell biology[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biophysics[SDV] Life Sciences [q-bio]Biological sciencesBiomolecular engineeringCELL-DEATHApoptosisCell culture030220 oncology & carcinogenesisTumor necrosis factor alphaBIOSENSORSHuman medicineiScience
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The MDM2-p53 pathway is involved in preconditioning-induced neuronal tolerance to ischemia

2018

Brain preconditioning (PC) refers to a state of transient tolerance against a lethal insult that can be evoked by a prior mild event. It is thought that PC may induce different pathways responsible for neuroprotection, which may involve the attenuation of cell damage pathways, including the apoptotic cell death. In this context, p53 is a stress sensor that accumulates during brain ischemia leading to neuronal death. The murine double minute 2 gene (MDM2), a p53-specific E3 ubiquitin ligase, is the main cellular antagonist of p53, mediating its degradation by the proteasome. Here, we study the role of MDM2-p53 pathway on PC-induced neuroprotection both in cultured neurons (in vitro) and rat …

Cell death0301 basic medicineProgrammed cell deathCell SurvivalNeuronalScience2415 Biología MolecularIschemiaNeuroprotectionArticleBrain ischemiaMiceBrain ischemia03 medical and health sciences0302 clinical medicineIschemiaXarxes neuronals (Neurobiologia)medicineAnimalsIschemic PreconditioningCell damageCells CulturedBrain preconditioningNeuronsMultidisciplinarybiologyChemistryQRBrainProto-Oncogene Proteins c-mdm2MDM2-p53medicine.diseaseNeuroprotectionRatsCell biologyUbiquitin ligaseDisease Models Animal030104 developmental biology2490 Neurocienciasbiology.proteinMedicineIschemic preconditioningMdm2Tumor Suppressor Protein p53030217 neurology & neurosurgerySignal Transduction
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Central and Peripheral Secondary Cell Death Processes after Transient Global Ischemia in Nonhuman Primate Cerebellum and Heart

2019

Cerebral ischemia and its pathological sequelae are responsible for severe neurological deficits generally attributed to the neural death within the infarcted tissue and adjacent regions. Distal brain regions, and even peripheral organs, may be subject to more subtle consequences of the primary ischemic event which can initiate parallel disease processes and promote comorbid symptomology. In order to characterize the susceptibility of cerebellar brain regions and the heart to transient global ischemia (TGI) in nonhuman primates (NHP), brain and heart tissues were harvested 6 months post-TGI injury. Immunostaining analysis with unbiased stereology revealed significant cell death in lobule II…

Cell deathInflammationPathologymedicine.medical_specialtyProgrammed cell deathCerebellumbusiness.industryPurkinje cellNeurodegenerationIschemiaInflammationStereologymedicine.diseaseSecondary injury03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureApoptosis030220 oncology & carcinogenesisMedicineNeurodegenerationmedicine.symptombusiness030217 neurology & neurosurgeryImmunostaining
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Onset of heart failure determines the hepatic cell death pattern.

2011

Background and rationale. Acute and chronic heart failure (HF) may affect the liver, but the underlying mechanisms that lead to progressive liver damage are poorly understood. The hepatic cytokeratin-18 (CK18) epitopes M65 and M30 have been reported to distinguish between overall (necrotic) and apoptotic cell death, respectively. We aimed to evaluate the predominant hepatic cell death pattern in acute vs. chronic heart failure and examined if these assays predict the course of the disease. Main results. In a prospective study comprising 21 patients with acute HF (AHF) and 18 patients with chronic HF (CHF) serum levels of M65 and M30 were assessed. Compared with CHF, M65 levels were signific…

Cell deathMalemedicine.medical_specialtyProgrammed cell deathMedizinM65Specialties of internal medicineApoptosisLiver injuryEpitopesPredictive Value of TestsInternal medicinemedicineHumansProspective StudiesProspective cohort studySurvival analysisHeart FailureLiver injuryKeratin-18HepatologyCytokeratin 18business.industryM30Liver DiseasesGeneral MedicineMiddle AgedPrognosismedicine.diseaseSurvival AnalysisRC581-951LiverApoptosisPredictive value of testsHeart failureAcute DiseaseChronic DiseaseHepatic stellate cellCardiologyFemalebusinessBiomarkers
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Human Hsp10 and Early Pregnancy Factor (EPF) and their relationship and involvement in cancer and immunity: current knowledge and perspectives.

2009

This article is about Hsp10 and its intracellular and extracellular forms focusing on the relationship of the latter with Early Pregnancy Factor and on their roles in cancer and immunity. Cellular physiology and survival are finely regulated and depend on the correct functioning of the entire set of proteins. Misfolded or unfolded proteins can cause deleterious effects and even cell death. The chaperonins Hsp10 and Hsp60 act together inside the mitochondria to assist protein folding. Recent studies demonstrated that these proteins have other roles inside and outside the cell, either together or independently of each other. For example, Hsp10 was found increased in the cytosol of different t…

Cell physiologyHsp10 tumor immunity chaperonins early pregnancy factor developmentProgrammed cell deathProtein Foldingmedicine.medical_treatmentBiologyPregnancy ProteinsGeneral Biochemistry Genetics and Molecular BiologyAutoimmune DiseasesImmune systemImmunityNeoplasmsExtracellularmedicineChaperonin 10Suppressor Factors ImmunologicHumansGeneral Pharmacology Toxicology and PharmaceuticsSettore BIO/16 - Anatomia UmanaGrowth factorGeneral MedicineCell biologyMitochondriaProtein TransportHSP60IntracellularLife sciences
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Resveratrol reduces oxidative stress and cell death and increases mitochondrial antioxidants and XIAP in PC6.3-cells.

2010

Resveratrol, a polyphenol derived e.g. from red grapes, has been shown to mediate several positive biological actions such as protection of cells against oxidative stress. It can also influence cell signaling, but the mechanisms behind its antioxidant properties are largely unknown. Here we show that RSV reduces oxidative stress and enhances cell survival in PC6.3 cells depending on the concentration. In these cells, RSV increased the levels of antioxidants, SOD2 and TRX2, and of X chromosome-linked inhibitor of apoptosis protein. RSV also activated NFκB signaling as shown using luciferase reporter constructs. These findings show that RSV regulates oxidative stress and mitochondrial antioxi…

Cell signalingProgrammed cell deathBlotting WesternSOD2Settore BIO/11 - Biologia MolecolareApoptosisX-Linked Inhibitor of Apoptosis ProteinMitochondrionBiologyResveratrolmedicine.disease_causeInhibitor of apoptosisSettore BIO/09 - FisiologiaPolymerase Chain ReactionAntioxidantsCell LineMitochondrial Proteins03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineThioredoxinsStilbenesmedicineTRX2Humans030304 developmental biologyNeurons0303 health sciencesSuperoxide DismutaseGeneral Neurosciencefood and beveragesROSSOD23. Good healthXIAPCell biologyMitochondriaOxidative StressBiochemistrychemistryResveratrolSettore BIO/14 - FarmacologiaOxidative stre030217 neurology & neurosurgeryOxidative stressNFκBNeuroscience letters
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PON3 is upregulated in cancer tissues and protects against mitochondrial superoxide-mediated cell death

2012

To achieve malignancy, cancer cells convert numerous signaling pathways, with evasion from cell death being a characteristic hallmark. The cell death machinery represents an anti-cancer target demanding constant identification of tumor-specific signaling molecules. Control of mitochondrial radical formation, particularly superoxide interconnects cell death signals with appropriate mechanistic execution. Superoxide is potentially damaging, but also triggers mitochondrial cytochrome c release. While paraoxonase (PON) enzymes are known to protect against cardiovascular diseases, recent data revealed that PON2 attenuated mitochondrial radical formation and execution of cell death. Another famil…

Cell signalingProgrammed cell deathMAP Kinase Signaling SystemApoptosisMitochondrionBiologyEndoplasmic ReticulumGene Expression Regulation EnzymologicMicechemistry.chemical_compoundSuperoxidesNeoplasmsAnimalsHumansMolecular BiologyOriginal PaperAryldialkylphosphataseSuperoxideCytochromes cCell BiologyMitochondriaNeoplasm ProteinsUp-RegulationCell biologyGene Expression Regulation NeoplasticHEK293 CellschemistryApoptosisCancer cellDNAJA3Signal transductionCell Death & Differentiation
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Differential regulation of the clusterin gene by Ha-ras and c-myc oncogenes and during apoptosis

1998

Clusterin (ApoJ) is an extracellular glycoprotein expressed during processes of tissue differentiation and regression that involve programmed cell death (apoptosis). Increased clusterin expression has also been found in tumors, however, the mechanism underlying this induction is not known. Apoptotic processes in tumors could be responsible for clusterin gene activation. Alternatively, oncogenic mutations could modulate signal transduction, thereby inducing the gene. We examined the response of the rat clusterin gene to two oncogenes, Ha-ras and c-myc, in transfected Rat1 fibroblasts. While c-myc overexpression did not modify clusterin gene activity, the Ha-ras oncogene produced a seven to t…

Cell signalingProgrammed cell deathUltraviolet RaysPhysiologyRecombinant Fusion ProteinsClinical BiochemistryGenes mycApoptosisDNA FragmentationBiologyTransfectionProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)AnimalsRNA MessengerCell Line TransformedGlycoproteinsOncogeneClusterinCell CycleCell BiologyTransfectionFibroblastsCell cycleeye diseasesRatsClusterinGenes rasApoptosisMutationCancer researchbiology.proteinsense organsSignal transductionMolecular ChaperonesSignal TransductionJournal of Cellular Physiology
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U937 variant cells as a model of apoptosis without cell disintegration

2012

AbstractThe variant cell line U937V was originally identified by a higher sensitivity to the cytocidal action of tumor necrosis factor alpha (TNFα) than that of its reference cell line, U937. We noticed that a typical morphological feature of dying U937V cells was the lack of cellular disintegration, which contrasts to the formation of apoptotic bodies seen with dying U937 cells. We found that both TNFα, which induces the extrinsic apoptotic pathway, and etoposide (VP-16), which induces the intrinsic apoptotic pathway, stimulated U937V cell death without cell disintegration. In spite of the distinct morphological differences between the U937 and U937V cells, the basic molecular events of ap…

Cell typeProgrammed cell deathBlotting WesternCellApoptosisU937 cellsDNA FragmentationBiologyModels BiologicalBiochemistrymedicineHumansCell ShapeMolecular BiologyU937 cellCytochrome cCytochromes chemic and immune systemsCell BiologyApoptotic bodyCaspase 9MitochondriaCell biologyEnzyme Activationmedicine.anatomical_structureApoptosisCell culturebiology.proteinApoptotic bodiesLymphoma Large B-Cell DiffuseCell disintegrationSignal TransductionResearch ArticleCellular and Molecular Biology Letters
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