Search results for "MITO"

showing 10 items of 2513 documents

Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress.

2012

7-Ketocholesterol (7-KC)-induced apoptosis of macrophages is considered a key event in the development of human atheromas. In the present study, the effect of indicaxanthin (Ind), a bioactive pigment from cactus pear fruit, on 7-KC-induced apoptosis of human monocyte/macrophage THP-1 cells was investigated. A pathophysiological condition was simulated by using amounts of 7-KC that can be reached in human atheromatous plaque. Ind was assayed within a micromolar concentration range, consistent with its plasma level after dietary supplementation with cactus pear fruit. Pro-apoptotic effects of 7-KC were assessed by cell cycle arrest, exposure of phosphatidylserine at the plasma membrane, varia…

Programmed cell deathPyridinesCellMedicine (miscellaneous)Apoptosismedicine.disease_causeMonocytesCell Linechemistry.chemical_compoundCytosolmedicineHumansSulfhydryl CompoundsKetocholesterolsNutrition and DieteticsChemistryPlant ExtractsMonocyteMacrophagesNF-kappa BNADPH OxidasesOpuntiaPhosphatidylserineAtherosclerosisPlaque AtheroscleroticCell biologyBetaxanthinsMitochondriaCytosolOxidative Stressmedicine.anatomical_structureApoptosisNADPH Oxidase 4FruitDietary SupplementsCalciumReactive Oxygen SpeciesIndicaxanthinOxidative stressPhytotherapyThe British journal of nutrition
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Kel1 is a phosphorylation-regulated noise suppressor of the pheromone signaling pathway.

2021

Abstract Mechanisms have evolved that allow cells to detect signals and generate an appropriate response. The accuracy of these responses relies on the ability of cells to discriminate between signal and noise. How cells filter noise in signaling pathways is not well understood. We have analyzed noise suppression in the yeast pheromone signaling pathway. By combining synthetic genetic array screening, mass spectrometry and single-cell time-resolved microscopy, we discovered that the poorly characterized protein Kel1 serves as a major noise suppressor of the pathway. At the molecular level, Kel1 suppresses spontaneous activation of the pheromone response by inhibiting membrane recruitment of…

Programmed cell deathSaccharomyces cerevisiae ProteinsChemistryCellbiologiCell BiologySaccharomyces cerevisiaeSynthetic genetic arrayGeneral Biochemistry Genetics and Molecular BiologyPheromonesCell biologylaw.inventionlawFus3SuppressorPhosphorylationPheromoneSignal transductionMitogen-Activated Protein KinasesPhosphorylationNoiseSte5Adaptor Proteins Signal TransducingCyclin-Dependent Kinase Inhibitor ProteinsSignal TransductionCell reports
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α-Tocopherol impairs 7-ketocholesterol-induced caspase-3-dependent apoptosis involving GSK-3 activation and Mcl-1 degradation on 158N murine oligoden…

2011

Abstract In important and severe neurodegenerative pathologies, 7-ketocholesterol, mainly resulting from cholesterol autoxidation, may contribute to dys- or demyelination processes. On various cell types, 7-ketocholesterol has often been shown to induce a complex mode of cell death by apoptosis associated with phospholipidosis. On 158N murine oligodendrocytes treated with 7-ketocholesterol (20 μg/mL corresponding to 50 μM, 24–48 h), the induction of a mode of cell death by apoptosis characterised by the occurrence of cells with condensed and/or fragmented nuclei, caspase activation (including caspase-3) and internucleosomal DNA fragmentation was observed. It was associated with a loss of tr…

Programmed cell deathTime FactorsCell Survivalalpha-TocopherolApoptosisCaspase 3BiochemistryDephosphorylationGlycogen Synthase Kinase 3MiceMembrane MicrodomainsGSK-3AnimalsKetocholesterolsMolecular BiologyProtein kinase BCell ProliferationMembrane Potential MitochondrialPhospholipidosisGlycogen Synthase Kinase 3 betaCaspase 3ChemistryOrganic ChemistryCytochromes cCell BiologyCell biologyEnzyme ActivationOligodendrogliaProtein TransportProto-Oncogene Proteins c-bcl-2ApoptosisMyeloid Cell Leukemia Sequence 1 ProteinDNA fragmentationChemistry and Physics of Lipids
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Mode of cell death induction by pharmacological Vacuolar H+-ATPase (V-ATPase) inhibition.

2012

The vacuolar H+-ATPase (V-ATPase), a multisubunit proton pump, has come into focus as an attractive target in cancer invasion. However, little is known about the role of V-ATPase in cell death, and especially the underlying mechanisms remain mostly unknown. We used the myxobacterial macrolide archazolid B, a potent inhibitor of the V-ATPase, as an experimental drug as well as a chemical tool to decipher V-ATPase-related cell death signaling. We found that archazolid induced apoptosis in highly invasive tumor cells at nanomolar concentrations which was executed by the mitochondrial pathway. Prior to apoptosis induction archazolid led to the activation of a cellular stress response including …

Programmed cell deathVacuolar Proton-Translocating ATPasesCellBiologyBiochemistryCellular stress responseCell Line TumormedicineAutophagyV-ATPaseHumansEnzyme InhibitorsMolecular BiologyCell ProliferationMembrane Potential MitochondrialMicroscopy ConfocalCell DeathCell growthAutophagyCytochromes cCell BiologyCell biologymedicine.anatomical_structureApoptosisSignal transductionSignal Transduction
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Calcitonin gene-related peptide partly protects cultured smooth muscle cells from apoptosis induced by an oxidative stress via activation of ERK1/2 M…

2003

Abstract Oxidative stress induced by a glucose/glucose oxidase (G/GO) generator system dose-dependently decreased the viability of cultured vascular smooth muscle cells (VSMC) as estimated by MTT assay. Cell death was induced in 40% of cells exposed to 0.2 IU/ml of the free radical generating mixture. Annexin-V labeling, Hoechst staining together with DNA laddering demonstrated that apoptosis was responsible for this cell loss. Pretreatment of the cells with 10−8 M calcitonin gene-related peptide (CGRP) significantly attenuated the damaging effect of the oxidative stress. Indeed, cell viability was estimated to be 80% in CGRP-treated group, instead of 60% in absence of CGRP treatment. This …

Programmed cell deathVascular smooth musclep38 mitogen-activated protein kinasesCalcitonin Gene-Related PeptideMyocytes Smooth MuscleApoptosisBiologyDNA ladderingCalcitonin gene-related peptidemedicine.disease_causeProtective AgentsMuscle Smooth VascularmedicineAnimalsHumansCGRPViability assayRats WistarMolecular BiologyCells CulturedMitogen-Activated Protein Kinase 3integumentary systemSAPKCell BiologyHydrogen PeroxideMAPKMolecular biologyRatsUp-RegulationNeuropeptideOxidative StressMitogen-activated protein kinaseVascular smooth muscle cellbiology.proteinMitogen-Activated Protein KinasesOxidative stressReceptors Calcitonin Gene-Related PeptideSignal TransductionBiochimica et biophysica acta
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Highlighting curcumin-induced crosstalk between autophagy and apoptosis: A biochemical approach coupling impedancemetry, imaging, and flow cytometry

2019

Curcumin, a major active component of turmeric (Curcuma longa, L.), is known to have various effects on both healthy and cancerous tissues. In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanism underlying the anticancer effects of curcumin is still unclear. Since there is a consensus about endoplasmic reticulum (ER) stress being involved in the cytotoxicity of many natural compounds, we investigated by Amnis ® Imaging flow cytome-try the mechanistic aspects of curcumin's destabilization of the ER, but also the status of the lysosomal compartment involved in curcumin-associated apoptosis. Curcumin induces ER stress thereby causing an un…

Programmed cell death[SDV]Life Sciences [q-bio][SDV.TOX.TVM]Life Sciences [q-bio]/Toxicology/Vegetal toxicology and mycotoxicology[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Mitochondrion03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biology0303 health sciencesChemistryAutophagy[SDV.BBM.MN]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular Networks [q-bio.MN]Cell cycle3. Good healthCell biology[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsApoptosis030220 oncology & carcinogenesis[SDV.TOX]Life Sciences [q-bio]/ToxicologyCancer cellUnfolded protein responseCurcumin
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Prevention by Dietary Polyphenols (Resveratrol, Quercetin, Apigenin) Against 7-Ketocholesterol-Induced Oxiapoptophagy in Neuronal N2a Cells: Potentia…

2020

The Mediterranean diet is associated with health benefits due to bioactive compounds such as polyphenols. The biological activities of three polyphenols (quercetin (QCT), resveratrol (RSV), apigenin (API)) were evaluated in mouse neuronal N2a cells in the presence of 7-ketocholesterol (7KC), a major cholesterol oxidation product increased in patients with age-related diseases, including neurodegenerative disorders. In N2a cells, 7KC (50 &micro

Programmed cell deathanimal diseasesSOD2N2a cellsApoptosisresveratrolmedicine.disease_causeoxiapoptophagyArticleCell LinequercetinMiceage-related diseasesmedicineAutophagyPeroxisomesAnimalsHumansApigeninlcsh:QH301-705.5Ketocholesterols7-ketocholesterolchemistry.chemical_classificationNeuronsReactive oxygen speciesDose-Response Relationship DrugChemistryfood and beveragesPolyphenolsNeurodegenerative DiseasesGeneral MedicinePeroxisomeMolecular biologyMitochondriaOxidative StresspolyphenolMitochondrial biogenesislcsh:Biology (General)ApoptosisACOX1Reactive Oxygen SpeciesoxysterolOxidative stressCells
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Highlighting Curcumin-Induced Crosstalk between Autophagy and Apoptosis as Supported by Its Specific Subcellular Localization

2020

Curcumin, a major active component of turmeric (Curcuma longa, L.), is known to have various effects on both healthy and cancerous tissues. In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanism underlying the anticancer effect of curcumin is still unclear. Since there is a recent consensus about endoplasmic reticulum (ER) stress being involved in the cytotoxicity of natural compounds, we have investigated using Image flow cytometry the mechanistic aspects of curcumin&rsquo

Programmed cell deathautophagyCell Membrane PermeabilityCurcumin[SDV]Life Sciences [q-bio][SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Article03 medical and health scienceschemistry.chemical_compound0302 clinical medicineLysosomeCell Line TumorxCELLigencemedicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Humanscancerlcsh:QH301-705.5030304 developmental biologyreal-time cellular impedanceCell Nucleus0303 health sciencescalciumEndoplasmic reticulumAutophagyapoptosisROSGeneral Medicine3. Good healthCell biologyMitochondriaendoplasmic reticulummedicine.anatomical_structurecell deathchemistrylcsh:Biology (General)Apoptosis030220 oncology & carcinogenesisCancer cellCurcuminUnfolded protein responseUnfolded Protein ResponselysosomeLysosomes[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologySubcellular Fractions
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Autophagy-Dependent Anticancer Immune Responses Induced by Chemotherapeutic Agents in Mice

2011

Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the release of adenosine triphosphate (ATP) from dying tumor cells. Conversely, inhibition of extracellular ATP-degrading enzymes increased pericellular ATP in autophagy-deficient tumors, reestablished the recr…

Programmed cell deathcells cancer immunogenicity calreticulin exposure hmgb1Antineoplastic AgentsBiologyimmunogenicityNOMicechemistry.chemical_compoundAdenosine TriphosphateImmune systemCell Line TumorNeoplasmsAutophagyExtracellularAnimalsHumanscancerMice Inbred BALB CMultidisciplinaryCell DeathImmunogenicityAutophagyDendritic CellsMice Inbred C57BLhmgb1chemistryCell cultureCancer researchImmunogenic cell deathcellsMitoxantroneCalreticulinAdenosine triphosphatecalreticulin exposure
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Death of mitochondria during programmed cell death of leaf mesophyll cells

2005

The role of plant mitochondria in the programmed cell death (PCD) is widely discussed. However, spectrum and sequence of mitochondrial structural changes during different types of PCD in leaves are poorly described. Pea, cucumber and rye plants were grown under controlled growing conditions. A part of them were sprinkled with ethylene releaser to accelerate cell death. During yellowing the palisade parenchyma mitochondria were attracted to nuclear envelope. Mitochondrial matrix became electron translucent. Mitochondria entered vacuole by invagination of tonoplast and formed multivesicular bodies. Ethephon treatment increased the frequency of sticking of mitochondria to the nuclear envelope …

Programmed cell deathfood and beveragesApoptosisCell BiologyGeneral MedicineVacuoleMitochondrionPeroxisomeGolgi apparatusBiologyMitochondriaCell biologyPlant LeavesChloroplastsymbols.namesakeOrganophosphorus CompoundsPlant Growth RegulatorsApoptosissymbolsUltrastructurePlant Physiological PhenomenaCell Biology International
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