Search results for "mitochondrial dynamic"

showing 10 items of 19 documents

Mitochondrial dynamics and metabolism in induced pluripotency.

2020

Somatic cells can be reprogrammed to pluripotency by either ectopic expression of defined factors or exposure to chemical cocktails. During reprogramming, somatic cells undergo dramatic changes in a wide range of cellular processes, such as metabolism, mitochondrial morphology and function, cell signaling pathways or immortalization. Regulation of these processes during cell reprograming lead to the acquisition of a pluripotent state, which enables indefinite propagation by symmetrical self-renewal without losing the ability of reprogrammed cells to differentiate into all cell types of the adult. In this review, recent data from different laboratories showing how these processes are control…

0301 basic medicineAdultAgingCell typeSomatic cellCellInduced Pluripotent Stem CellsBiologyBiochemistryMitochondrial Dynamics03 medical and health sciences0302 clinical medicineEndocrinologyGeneticsmedicineHumansInduced pluripotent stem cellMolecular BiologyCell DifferentiationCell BiologyCellular ReprogrammingPhenotypeCell biology030104 developmental biologymedicine.anatomical_structureEctopic expressionReprogramming030217 neurology & neurosurgeryFunction (biology)Signal TransductionExperimental gerontology
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Are Mitochondrial Fusion and Fission Impaired in Leukocytes of Type 2 Diabetic Patients?

2016

Mitochondrial fusion/fission alterations have been evaluated in different tissues of type 2 diabetic (T2D) patients. However, it is not known whether mitochondrial dynamics is disturbed in the leukocytes of T2D patients and whether glycemic control affects its regulation. Anthropometric and metabolic parameters in 91 T2D patients (48 with glycated hemoglobin [HbA1c]6.5% and 43 with HbA1c6.5%) were characteristic of the disease when compared with 78 control subjects. We observed increased reactive oxygen species production in leukocytes from diabetic patients, together with a reduced mitochondrial oxygen consumption rate, especially in poorly controlled patients. Mitochondrial fusion was red…

0301 basic medicineAdultMalemedicine.medical_specialtyendocrine system diseasesEndotheliumPhysiologyClinical BiochemistryCell CommunicationBiologymedicine.disease_causeBiochemistryMitochondrial DynamicsMitochondrial Membrane Transport Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineDiabetes mellitusmedicineLeukocytesHumansMolecular BiologyGeneral Environmental ScienceGlycemicAgedCase-control studyIncreased reactive oxygen species productionCell BiologyMiddle Agedmedicine.diseaseMitochondriaOxidative Stress030104 developmental biologyEndocrinologymedicine.anatomical_structuremitochondrial fusionchemistryDiabetes Mellitus Type 2Gene Expression Regulation030220 oncology & carcinogenesisCase-Control StudiesGeneral Earth and Planetary SciencesFemaleGlycated hemoglobinEndothelium VascularReactive Oxygen SpeciesOxidative stressBiomarkersAntioxidantsredox signaling
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Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo.

2018

Mitochondrial dysfunction plays an important role in the etiology of age-related muscle atrophy known as sarcopenia. PGC-1α is positioned at the center of crosstalk in regulating mitochondrial quality control, but its role in mitophagy in aged skeletal muscle is currently unclear. The present study investigated the effects of aging and PGC-1α overexpression via in vivo DNA transfection on key mitophagy protein markers, as well as mitochondrial dynamics related proteins, metabolic function and antioxidant capacity in mouse muscle. C57BL/6J mice at the age of 2 mo (young, Y; N = 14) and 24 mo (old, O; N = 14) were transfected in vivo with either PGC-1α DNA (OE, N = 7) or GFP (N = 7) into the …

0301 basic medicineAgingUbiquitin-Protein LigasesPINK1MitochondrionBiochemistryMitochondrial DynamicsGTP Phosphohydrolases03 medical and health sciencesMice0302 clinical medicineIn vivoPhysiology (medical)MitophagymedicineAnimalsMuscle SkeletalChemistryMitophagySkeletal muscleTransfectionmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMuscle atrophyCell biologyMitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structureGene Expression RegulationSarcopeniaBeclin-1medicine.symptomProtein Kinases030217 neurology & neurosurgeryFree radical biologymedicine
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MYC Induces a Hybrid Energetics Program Early in Cell Reprogramming

2018

Summary Cell reprogramming is thought to be associated with a full metabolic switch from an oxidative- to a glycolytic-based metabolism. However, neither the dynamics nor the factors controlling this metabolic switch are fully understood. By using cellular, biochemical, protein array, metabolomic, and respirometry analyses, we found that c-MYC establishes a robust bivalent energetics program early in cell reprogramming. Cells prone to undergo reprogramming exhibit high mitochondrial membrane potential and display a hybrid metabolism. We conclude that MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming, whereby somatic cells acquire the phenotypic plast…

0301 basic medicineCell signalingSomatic cellCèl·lulesCellOxidative phosphorylationcell reprogramming cell signaling metabolism mitochondrial dynamicsBiologyHybrid CellsBiochemistryMitochondrial DynamicsArticleOxidative PhosphorylationMitocondrisProto-Oncogene Proteins c-myc03 medical and health sciencesMetabolomicsCDC2 Protein KinaseGeneticsmedicinecell signalingAnimalsHumansGlycolysisPhosphorylationlcsh:QH301-705.5Membrane potentialMembrane Potential Mitochondriallcsh:R5-920cell reprogrammingCell BiologyCellular ReprogrammingCell biologyMitochondriaMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:Medicine (General)ReprogrammingmetabolismGlycolysisDevelopmental Biology
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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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A Crucial Role of Mitochondrial Dynamics in Dehydration Resistance in Saccharomyces cerevisiae

2021

Mitochondria are dynamic organelles as they continuously undergo fission and fusion. These dynamic processes conduct not only mitochondrial network morphology but also activity regulation and quality control. Saccharomyces cerevisiae has a remarkable capacity to resist stress from dehydration/rehydration. Although mitochondria are noted for their role in desiccation tolerance, the mechanisms underlying these processes remains obscure. Here, we report that yeast cells that went through stationary growth phase have a better survival rate after dehydration/rehydration. Dynamic defective yeast cells with reduced mitochondrial genome cannot maintain the mitochondrial activity and survival rate o…

0301 basic medicineMitochondrial DNASaccharomyces cerevisiae ProteinsQH301-705.5030106 microbiologySaccharomyces cerevisiaeSaccharomyces cerevisiaeMitochondrionyeastMitochondrial DynamicsCatalysisArticleInorganic ChemistryDesiccation tolerance03 medical and health sciencesmedicineDehydrationPhysical and Theoretical ChemistryBiology (General)DesiccationMolecular BiologyQD1-999SpectroscopyMicrobial ViabilitybiologyDehydrationChemistryOrganic ChemistryCell CycleWild typeGeneral Medicinedynamicsmedicine.diseasebiology.organism_classificationYeastComputer Science ApplicationsCell biologyMitochondriaChemistry030104 developmental biologymitochondrial fusionGenome MitochondrialInternational Journal of Molecular Sciences
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The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and cilia to regulate ciliogenesis and ciliary protein traffic

2022

ELMODs are a family of three mammalian paralogs that display GTPase activating protein (GAP) activity towards a uniquely broad array of ADP-ribosylation factor (ARF) family GTPases that includes ARF-like (ARL) proteins. ELMODs are ubiquitously expressed in mammalian tissues, highly conserved across eukaryotes, and ancient in origin, being present in the last eukaryotic common ancestor. We described functions of ELMOD2 in immortalized mouse embryonic fibroblasts (MEFs) in the regulation of cell division, microtubules, ciliogenesis, and mitochondrial fusion. Here, using similar strategies with the paralogs ELMOD1 and ELMOD3, we identify novel functions and locations of these cell regulators a…

Cell divisionGTPase-activating proteinGolgi ApparatusGTPaseBiologyMicrotubulesMitochondrial Dynamicssymbols.namesakeMiceMicrotubuleCiliogenesisAnimalsCiliaMolecular BiologyADP-Ribosylation FactorsCiliumGTPase-Activating ProteinsCorrectionCell BiologyGolgi apparatusFibroblastsCell biologyCytoskeletal Proteinsmitochondrial fusionsymbolsSignal Transduction
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c-MYC Triggers Lipid Remodelling During Early Somatic Cell Reprogramming to Pluripotency.

2021

AbstractMetabolic rewiring and mitochondrial dynamics remodelling are hallmarks of cell reprogramming, but the roles of the reprogramming factors in these changes are not fully understood. Here we show that c-MYC induces biosynthesis of fatty acids and increases the rate of pentose phosphate pathway. Time-course profiling of fatty acids and complex lipids during cell reprogramming using lipidomics revealed a profound remodelling of the lipid content, as well as the saturation and length of their acyl chains, in a c-MYC-dependent manner. Pluripotent cells displayed abundant cardiolipins and scarce phosphatidylcholines, with a prevalence of monounsaturated acyl chains. Cells undergoing cell r…

ChemistryCell growthCèl·lulesMetabolismPentose phosphate pathwayMitochondrionCellular ReprogrammingLipidsMitochondrial DynamicsArticleCell biologyCell membranePentose Phosphate Pathwaymedicine.anatomical_structuremedicineGlycolysisCàncerReprogrammingGlycolysisIntracellularStem cell reviews and reports
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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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Hypothalamic glucose sensing : mitochondrial dynamic involument in reactive oxygen species signaling

2011

Energetic homeostasis results in the balance between energy intake and expenditure. The hypothalamus plays an important role in the regulation of both energetic metabolism and food intake in sensing hormonal and metabolic signals. For instance, changes in hypothalamic glucose level modulate food intake and insulin secretion. We have previously found that 1) increased hypothalamic glucose level triggers production of mitochondrial reactive oxygen species (mROS) from the electron transport chain; 2) hypothalamic mROS production is involved in glucose homeostasis and food intake control. The molecular mechanisms involved in glucose-induced hypothalamic mROS production are still unknown. Mitoch…

Energetic homeostasis[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyHypothalamusGlucose sensingMitochondrial dynamicsEspèces Actives de l’Oxygène mitochondriales (mEAOs)Homéostasie énergétiqueDétection du glucoseDynamique mitochondrialeReactive Oxygen Species (mROS)
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