Search results for "Dynamins"

showing 9 items of 9 documents

Effect of colorectal cancer-derived extracellular vesicles on the immunophenotype and cytokine secretion profile of monocytes and macrophages.

2018

Abstract. Background Macrophages are one of the most important players in the tumor microenvironment. The polarization status of tumor associated macrophages into a pro-inflammatory type M1 or anti-inflammatory type M2 may influence cancer progression and patient survival. Extracellular vesicles (EVs) are membrane-bound vesicles containing different biomolecules that are involved in cell to cell signal transfer. Accumulating evidence suggests that cancer-derived EVs are taken up by macrophages and modulate their phenotype and cytokine profile. However, the interactions of cancer-derived EVs with monocytes and macrophages at various differentiation and polarization states are poorly understo…

0301 basic medicineDynaminsLipopolysaccharidesCell SurvivalCD14Macrophage polarizationLipopolysaccharide ReceptorsShort Reportlcsh:MedicineReceptors Cell Surfacecolorectal cancerBiochemistryMonocytesImmunophenotyping03 medical and health sciencesExtracellular VesiclesInterferon-gamma0302 clinical medicineCell Line TumormedicineCXCL10MacrophageHumansendocytosisSecretionLectins C-Typelcsh:QH573-671Molecular BiologyTumor microenvironmentlcsh:CytologyChemistryMonocyteMacrophageslcsh:RCell DifferentiationCell BiologyHLA-DR AntigenscytokinesCell biology030104 developmental biologymedicine.anatomical_structureMannose-Binding Lectins030220 oncology & carcinogenesisTetradecanoylphorbol AcetateCytokine secretionChemokinesColorectal NeoplasmsMannose ReceptorCell communication and signaling : CCS
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Echovirus 1 Entry into Polarized Caco-2 Cells Depends on Dynamin, Cholesterol, and Cellular Factors Associated with Macropinocytosis

2013

ABSTRACT Enteroviruses invade their hosts by crossing the intestinal epithelium. We have examined the mechanism by which echovirus 1 (EV1) enters polarized intestinal epithelial cells (Caco-2). Virus binds to VLA-2 on the apical cell surface and moves rapidly to early endosomes. Using inhibitory drugs, dominant negative mutants, and small interfering RNAs (siRNAs) to block specific endocytic pathways, we found that virus entry requires dynamin GTPase and membrane cholesterol but is independent of both clathrin- and caveolin-mediated endocytosis. Instead, infection requires factors commonly associated with macropinocytosis, including amiloride-sensitive Na + /H + exchange, protein kinase C, …

DynaminsSodium-Hydrogen ExchangersEndosomeImmunologyEndocytic cycleEndocytosisMicrobiologyClathrinViral entryVirologyHumansTransport VesiclesProtein Kinase CDynaminbiologyPinocytosisEpithelial CellsVirus InternalizationIntestinal epitheliumEnterovirus B HumanVirus-Cell InteractionsCell biologyDNA-Binding ProteinsAlcohol OxidoreductasesCholesterolInsect ScienceHost-Pathogen Interactionsbiology.proteinPinocytosisCaco-2 CellsJournal of Virology
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Loss of endocytic clathrin-coated pits upon acute depletion of phosphatidylinositol 4,5-bisphosphate.

2007

Phosphatidylinositol 4,5-bisphosphate [PI(4,5) P 2 ], a phosphoinositide concentrated predominantly in the plasma membrane, binds endocytic clathrin adaptors, many of their accessory factors, and a variety of actin-regulatory proteins. Here we have used fluorescent fusion proteins and total internal reflection fluorescence microscopy to investigate the effect of acute PI(4,5) P 2 breakdown on the dynamics of endocytic clathrin-coated pit components and of the actin regulatory complex, Arp2/3. PI(4,5) P 2 breakdown was achieved by the inducible recruitment to the plasma membrane of an inositol 5-phosphatase module through the rapamycin/FRB/FKBP system or by treatment with ionomycin. PI(4,5)…

DynaminsPhosphatidylinositol 45-DiphosphateEpsinEndocytic cyclemacromolecular substancesEndocytosisClathrinClathrin coatModels Biologicalchemistry.chemical_compoundChlorocebus aethiopsAnimalsHumansDynaminSirolimusMultidisciplinarybiologyCell MembraneClathrin-Coated VesiclesBiological SciencesActinsEndocytosisCell biologyAdaptor Proteins Vesicular TransportPhosphatidylinositol 45-bisphosphatechemistryActin-Related Protein 3Actin-Related Protein 2COS Cellsbiology.proteinLamellipodiumProceedings of the National Academy of Sciences of the United States of America
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Early ERK1/2 activation promotes DRP1-dependent mitochondrial fission necessary for cell reprogramming.

2016

During the process of reprogramming to induced pluripotent stem (iPS) cells, somatic cells switch from oxidative to glycolytic metabolism, a transition associated with profound mitochondrial reorganization. Neither the importance of mitochondrial remodelling for cell reprogramming, nor the molecular mechanisms controlling this process are well understood. Here, we show that an early wave of mitochondrial fragmentation occurs upon expression of reprogramming factors. Reprogramming-induced mitochondrial fission is associated with a minor decrease in mitochondrial mass but not with mitophagy. The pro-fission factor Drp1 is phosphorylated early in reprogramming, and its knockdown and inhibition…

0301 basic medicineDynaminsSomatic cellMAP Kinase Signaling SystemScienceCèl·lulesCellInduced Pluripotent Stem CellsKruppel-Like Transcription FactorsGeneral Physics and AstronomyBiologyMitochondrionMitochondrial DynamicsGeneral Biochemistry Genetics and Molecular BiologyMitocondrisArticleCell LineProto-Oncogene Proteins c-myc03 medical and health sciencesKruppel-Like Factor 4MiceMitophagymedicineAnimalsPhosphorylationInduced pluripotent stem cellGeneticsMultidisciplinarySOXB1 Transcription FactorsQGeneral ChemistryCellular ReprogrammingCell biologyMitochondria030104 developmental biologymedicine.anatomical_structurePhosphorylationMitochondrial fissionReprogrammingOctamer Transcription Factor-3Nature communications
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PD‐1‐induced T cell exhaustion is controlled by a Drp1‐dependent mechanism

2022

Programmed cell death‐1 (PD‐1) signaling downregulates the T‐cell response, promoting an exhausted state in tumor‐infiltrating T cells, through mostly unveiled molecular mechanisms. Dynamin‐related protein‐1 (Drp1)‐dependent mitochondrial fission plays a crucial role in sustaining T‐cell motility, proliferation, survival, and glycolytic engagement. Interestingly, such processes are exactly those inhibited by PD‐1 in tumor‐infiltrating T cells. Here, we show that PD‐1pos CD8+ T cells infiltrating an MC38 (murine adenocarcinoma)‐derived murine tumor mass have a downregulated Drp1 activity and more elongated mitochondria compared with PD‐1neg counterparts. Also, PD‐1pos lymphocytic elements in…

DynaminsCancer Researchendocrine systemSettore BIO/06T cellmedicine.medical_treatmentProgrammed Cell Death 1 ReceptorDrp1CD8-Positive T-LymphocytesSettore MED/08 - Anatomia PatologicaMitochondrial Dynamicstumor‐infiltrating lymphocytesMiceImmune systemDownregulation and upregulationDrp1 mitochondria PD-1 T cell tumor-infiltrating lymphocytesPD-1GeneticsmedicineAnimalsHumansSettore MED/05 - Patologia ClinicaResearch ArticlesPI3K/AKT/mTOR pathwayRC254-282Tumor-infiltrating lymphocytesChemistryPD‐1T cellNeoplasms. Tumors. Oncology. Including cancer and carcinogensGeneral MedicineImmunotherapyCell biologymitochondriamedicine.anatomical_structureOncologytumor-infiltrating lymphocytesMolecular MedicineMitochondrial fissionCD8Research ArticleMolecular Oncology
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Tissue factor prothrombotic activity is regulated by integrin-arf6 trafficking

2017

Objective— Coagulation initiation by tissue factor (TF) is regulated by cellular inhibitors, cell surface availability of procoagulant phosphatidylserine, and thiol-disulfide exchange. How these mechanisms contribute to keeping TF in a noncoagulant state and to generating prothrombotic TF remain incompletely understood. Approach and Results— Here, we study the activation of TF in primary macrophages by a combination of pharmacological, genetic, and biochemical approaches. We demonstrate that primed macrophages effectively control TF cell surface activity by receptor internalization. After cell injury, ATP signals through the purinergic receptor P2rx7 induce release of TF + microvesicles. T…

0301 basic medicinedynaminsIntegrin alpha4CellCardiorespiratory Medicine and Haematology030204 cardiovascular system & hematologyIntegrin alpha4beta1Inbred C57BLTransgenicMicechemistry.chemical_compound0302 clinical medicineAdenosine TriphosphateCell-Derived MicroparticlesReceptors2.1 Biological and endogenous factorsfibrinGene Knock-In TechniquesAetiologyPhospholipidsTumorbiologyChemistryADP-Ribosylation FactorsHematologyPhosphatidylserineCell biologyProtein Transportmedicine.anatomical_structurePhenotypeProteomeextracellular vesiclesCardiology and Cardiovascular MedicinePurinergic P2X7BiotechnologySignal TransductionGenotypeproteomeClinical SciencesIntegrinMice TransgenicFactor VIIaTransfectionExtracellular vesiclesFibrinArticleCell LineThromboplastin03 medical and health sciencesTissue factorCell Line TumormedicineAnimalsHumansBlood CoagulationMacrophagesThrombosisMice Inbred C57BL030104 developmental biologyCardiovascular System & HematologyADP-Ribosylation Factor 6biology.proteinReceptors Purinergic P2X7
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Importance of mitochondrial dynamin-related protein 1 in hypothalamic glucose sensitivity in rats.

2012

International audience; AIMS: Hypothalamic mitochondrial reactive oxygen species (mROS)-mediated signaling has been recently shown to be involved in the regulation of energy homeostasis. However, the upstream signals that control this mechanism have not yet been determined. Here, we hypothesize that glucose-induced mitochondrial fission plays a significant role in mROS-dependent hypothalamic glucose sensing. RESULTS: Glucose-triggered translocation of the fission protein dynamin-related protein 1 (DRP1) to mitochondria was first investigated in vivo in hypothalamus. Thus, we show that intracarotid glucose injection induces the recruitment of DRP1 to VMH mitochondria in vivo. Then, expressio…

MaleEnergy-Generating Resourcesnervous-systemPhysiology[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionClinical BiochemistryneuronsMitochondrionBiochemistryinvolvementEnergy homeostasisDNM1L0302 clinical medicineInsulin-Secreting CellsInsulin SecretionInsulinGeneral Environmental Science2. Zero hungerchemistry.chemical_classification0303 health sciencesTransport proteinMitochondriaProtein TransportHypothalamusGene Knockdown TechniquesMitochondrial MembranesMitochondrial fissionRNA InterferenceDynaminsmedicine.medical_specialtyendocrine systembrainmechanismCarbohydrate metabolismBiology03 medical and health sciencesOxygen ConsumptionInternal medicineexpressionmedicineAnimalsRats WistarMolecular Biologyenergy homeostasis030304 developmental biologyReactive oxygen speciesAppetite RegulationArcuate Nucleus of HypothalamusCell Biologyislet blood-flowRatsEndocrinologyGlucosechemistryVentromedial Hypothalamic NucleusGeneral Earth and Planetary SciencesactivationReactive Oxygen Species[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryinsulin-secretion
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Inflammation-Induced Alteration of Astrocyte Mitochondrial Dynamics Requires Autophagy for Mitochondrial Network Maintenance

2013

Accumulating evidence suggests that changes in the metabolic signature of astrocytes underlie their response to neuroinflammation, but how proinflammatory stimuli induce these changes is poorly understood. By monitoring astrocytes following acute cortical injury, we identified a differential and region-specific remodeling of their mitochondrial network: while astrocytes within the penumbra of the lesion undergo mitochondrial elongation, those located in the core-the area invaded by proinflammatory cells-experience transient mitochondrial fragmentation. In brain slices, proinflammatory stimuli reproduced localized changes in mitochondrial dynamics, favoring fission over fusion. This effect w…

MaleLipopolysaccharidesPhysiologyDnm1l protein mouseInterleukin-1betaNitric Oxide Synthase Type IIMitochondrionAstrocytes/metabolismMitochondrial DynamicsAutophagy-Related Protein 7Mice0302 clinical medicinemetabolism [Reactive Oxygen Species]PhosphorylationCells Culturedcytology [Astrocytes]0303 health sciencesmetabolism [Inflammation]metabolism [Astrocytes]Inflammation/metabolismCytokines/metabolismdrug effects [Mitochondria]Mitochondria/drug effectsMitochondriaCell biologyAstrocytes/drug effectsmedicine.anatomical_structureMicrotubule-Associated Proteins/metabolismPhosphorylationCytokinesmetabolism [Dynamins]Nitric Oxide Synthase Type II/metabolismMicrotubule-Associated ProteinsAstrocytegenetics [Microtubule-Associated Proteins]DynaminsProgrammed cell deathAstrocytes/cytologydrug effects [Astrocytes]Mice TransgenicBiologypharmacology [Interferon-gamma]Proinflammatory cytokine03 medical and health sciencesInterferon-gammametabolism [Interleukin-1beta]reactive astrocytesReactive Oxygen Species/metabolismddc:570Mitochondria/metabolismtoxicity [Lipopolysaccharides]medicineAutophagyAnimalsAutophagy-Related Protein 7Molecular BiologyNeuroinflammation030304 developmental biologypathology [Inflammation]Dynamins/metabolismInflammationdrug effects [Mitochondrial Dynamics]Autophagymetabolism [Cytokines]Interferon-gamma/pharmacologyCell Biologymetabolism [Microtubule-Associated Proteins]Microtubule-Associated Proteins/geneticsMitochondrial Dynamics/drug effectsmetabolism [Mitochondria]metabolism [Nitric Oxide Synthase Type II]Mice Inbred C57BLLipopolysaccharides/toxicityAtg7 protein mouseAstrocytesInterleukin-1beta/metabolismReactive Oxygen Species030217 neurology & neurosurgeryInflammation/pathologyCell Metabolism
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Drp1 Controls Effective T Cell Immune-Surveillance by Regulating T Cell Migration, Proliferation, and cMyc-Dependent Metabolic Reprogramming

2018

Summary Mitochondria are key players in the regulation of T cell biology by dynamically responding to cell needs, but how these dynamics integrate in T cells is still poorly understood. We show here that the mitochondrial pro-fission protein Drp1 fosters migration and expansion of developing thymocytes both in vitro and in vivo. In addition, we find that Drp1 sustains in vitro clonal expansion and cMyc-dependent metabolic reprogramming upon activation, also regulating effector T cell numbers in vivo. Migration and extravasation defects are also exhibited in Drp1-deficient mature T cells, unveiling its crucial role in controlling both T cell recirculation in secondary lymphoid organs and acc…

Genetics and Molecular Biology (all)0301 basic medicinecell migrationT-LymphocytesCellCell CountMitochondrionLymphocyte ActivationBiochemistryCell MovementHomeostasismetabolic reprogrammingcell migration; cell proliferation; cMyc; Drp1; exhaustion; metabolic reprogramming; mitochondrial dynamics; T cells; thymocytes; tumor immune-surveillance; Biochemistry Genetics and Molecular Biology (all)lcsh:QH301-705.5cMycImmunologic SurveillanceMice KnockoutThymocytesEffectorDrp1; T cells; cMyc; cell migration; cell proliferation; exhaustion; metabolic reprogramming; mitochondrial dynamics; thymocytes; tumor immune-surveillanceCell migrationCell DifferentiationCell biologymedicine.anatomical_structurePhenotypeDynaminsendocrine systemSettore BIO/06Cell SurvivalLymphoid TissueMAP Kinase Signaling SystemT cellT cellsReceptors Antigen T-CellDrp1BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleProto-Oncogene Proteins c-myc03 medical and health sciencestumor immune-surveillancemitochondrial dynamicexhaustionHomeostasimedicineAnimalsCell ProliferationTumor microenvironmentBiochemistry Genetics and Molecular Biology (all)Cell growthAnimalT cellthymocytemitochondrial dynamicsDynamin030104 developmental biologylcsh:Biology (General)T-LymphocyteT cell migration
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