Search results for "MITOCHONDRION"

showing 10 items of 491 documents

Melatonin enhances neural stem cell differentiation and engraftment by increasing mitochondrial function

2017

Mendivil-Perez, Miguel et al.

0301 basic medicineMaleParkinson's diseaseCellMice TransgenicBiologyMitochondrionTransplantmedicine.disease_causeMelatonin03 medical and health sciencesMice0302 clinical medicineEndocrinologyAlzheimer DiseasemedicineAnimalsreproductive and urinary physiologyMelatoninNeuronsNeural stem cellsATP synthaseGraft SurvivalCell Differentiationmedicine.diseaseAntigens DifferentiationNeural stem cellnervous system diseasesCell biologyMitochondriaTransplantation030104 developmental biologymedicine.anatomical_structurenervous systemOxidative stressbiology.proteinParkinson’s diseaseNeuroscienceAlzheimer’s disease030217 neurology & neurosurgeryOxidative stressmedicine.drug
researchProduct

Short-Term Effects of Microglia-Specific Mitochondrial Dysfunction on Amyloidosis in Transgenic Models of Alzheimer's Disease.

2018

Reduction of mitochondrial activity is a subtle and early event in the pathogenesis of Alzheimer’s disease. Mitochondrial damage and consequentially enhanced production of reactive oxygen species is particularly occurring in the vicinity of amyloid plaques. Since all cells are affected by mitochondrial damage, analyses of cell type-specific effects are challenging. To study the impact of mitochondrial alterations on microglial activity in a homogeneous genetic background, we generated bone marrow chimeras of irradiated 46-days-old APP-transgenic mice. For reconstitution, bone marrow from CX3CR1-eGFP mice with mitochondria of either non-obese diabetic or C57BL/6J animals was utilized. Succes…

0301 basic medicineMalePathologymedicine.medical_specialtyMitochondrial DiseasesAmyloidCellGreen Fluorescent ProteinsCX3C Chemokine Receptor 1Mice TransgenicPlaque AmyloidBiologyMitochondrionPathogenesis03 medical and health sciencesAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseMice Inbred NODCX3CR1medicinePresenilin-1AnimalsHumansMicrogliaGeneral NeuroscienceAmyloidosisCalcium-Binding ProteinsMicrofilament ProteinsGeneral MedicineAmyloidosismedicine.diseaseMitochondriaMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureFemaleBone marrowMicrogliaGeriatrics and Gerontology030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
researchProduct

Mitochondrial Fatty Acid β-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish.

2020

BACKGROUND: Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. OBJECTIVES: This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. M…

0301 basic medicineMaleProtein metabolismMedicine (miscellaneous)MitochondrionEnergy homeostasis03 medical and health scienceschemistry.chemical_compoundNile tilapia0302 clinical medicineAdjuvants ImmunologicmedicineAnimalsHomeostasisInsulinCarnitineProtein kinase ACells CulturedZebrafishNutrition and DieteticsbiologyCarnitine O-PalmitoyltransferaseChemistryFatty AcidsProtein turnoverProteinsMetabolismCichlidsDNACytochromes bbiology.organism_classificationMitochondria030104 developmental biologyGlucoseBiochemistryMutationHepatocytesNutrient Physiology Metabolism and Nutrient-Nutrient InteractionsEnergy MetabolismOxidation-Reduction030217 neurology & neurosurgerymedicine.drugMethylhydrazinesThe Journal of nutrition
researchProduct

Mitochondrial Changes in β0-Thalassemia/Hb E Disease.

2015

The compound β°-thalassemia/Hb E hemoglobinopathy is characterized by an unusually large range of presentation from essentially asymptomatic to a severe transfusion dependent state. While a number of factors are known that moderate presentation, these factors do not account for the full spectrum of presentation. Mitochondria are subcellular organelles that are pivotal in a number of cellular processes including oxidative phosphorylation and apoptosis. A mitochondrial protein enriched proteome was determined and validated from erythroblasts from normal controls and β°-thalassemia/Hb E patients of different severities. Mitochondria were evaluated through the use of mitotracker staining, analy…

0301 basic medicineMetabolic ProcessesErythroblastsProteomeProteomesCelllcsh:MedicineGene ExpressionAntigens CD34ApoptosisMitochondrionBiochemistryOxidative Phosphorylation0302 clinical medicineAnimal Cellshemic and lymphatic diseasesRed Blood CellsGene expressionlcsh:ScienceErythroid Precursor CellsEnergy-Producing OrganellesErythroid Precursor CellsStainingMultidisciplinaryCell DeathHemoglobin ECell StainingCell biologyGlobinsMitochondriamedicine.anatomical_structureCell Processes030220 oncology & carcinogenesisCellular Structures and OrganellesCellular TypesResearch ArticleMitochondrial DNAPrecursor CellsBone Marrow CellsOxidative phosphorylationBiologyBioenergeticsResearch and Analysis Methods03 medical and health sciencesmedicineHumansGlobinBlood Cellslcsh:Rbeta-ThalassemiaBiology and Life SciencesProteinsCell BiologyMolecular biologyChaperone ProteinsHemoglobinopathies030104 developmental biologyMetabolismApoptosisSpecimen Preparation and TreatmentCase-Control Studieslcsh:QPloS one
researchProduct

Dysfunctional mitochondrial fission impairs cell reprogramming

2016

We have recently shown that mitochondrial fission is induced early in reprogramming in a Drp1-dependent manner; however, the identity of the factors controlling Drp1 recruitment to mitochondria was unexplored. To investigate this, we used a panel of RNAi targeting factors involved in the regulation of mitochondrial dynamics and we observed that MiD51, Gdap1 and, to a lesser extent, Mff were found to play key roles in this process. Cells derived from Gdap1-null mice were used to further explore the role of this factor in cell reprogramming. Microarray data revealed a prominent down-regulation of cell cycle pathways in Gdap1-null cells early in reprogramming and cell cycle profiling uncovered…

0301 basic medicineMicroarray analysis techniquescell reprogrammingmitochondrial fissionCellCell BiologyBiologyMitochondrionCell cyclepluripotencyCell biology03 medical and health sciencesiPS cells030104 developmental biology0302 clinical medicinemedicine.anatomical_structureRNA interferencemedicineMitochondrial fissionGdap1Induced pluripotent stem cellMolecular BiologyReprogramming030217 neurology & neurosurgeryDevelopmental Biology
researchProduct

The purine analogues abacavir and didanosine increase acetaminophen-induced hepatotoxicity by enhancing mitochondrial dysfunction

2016

Background NRTIs are essential components of HIV therapy with well-documented, long-term mitochondrial toxicity in hepatic cells, but whose acute effects on mitochondria are unclear. As acetaminophen-induced hepatotoxicity also involves mitochondrial interference, we hypothesized that it would be exacerbated in the context of ART. Methods We evaluated the acute effects of clinically relevant concentrations of the most widely used NRTIs, alone or combined with acetaminophen, on mitochondrial function and cellular viability. Results The purine analogues abacavir and didanosine produced an immediate and concentration-dependent inhibition of oxygen consumption and complex I and III activity. Th…

0301 basic medicineMicrobiology (medical)Mitochondrial DiseasesstavudineAnti-HIV Agentsantiretroviral therapyPurine analogueContext (language use)Mitochondria LiverMitochondrionPharmacologymedicine.disease_causeacute liver-failureCell Line03 medical and health sciencesOxygen ConsumptionmedicineHumansPharmacology (medical)Reverse-transcriptase inhibitorsAcetaminophenPharmacologychemistry.chemical_classificationmechanismsReactive oxygen speciesbusiness.industryassociationtoxicityAnalgesics Non-Narcoticmedicine.diseaseGlutathioneReactive Nitrogen SpeciesDideoxynucleosideshep3b cellsAcetaminophenMitochondrial toxicityDidanosine030104 developmental biologyInfectious DiseaseschemistryElectron Transport Chain Complex ProteinsToxicityhypersensitivityChemical and Drug Induced Liver Injurybusinesshepatic cellsOxidative stressmedicine.drug
researchProduct

C2orf69 mutations disrupt mitochondrial function and cause a multisystem human disorder with recurring autoinflammation

2021

BACKGROUND. Deciphering the function of the many genes previously classified as uncharacterized open reading frame (ORF) would complete our understanding of a cell’s function and its pathophysiology. METHODS. Whole-exome sequencing, yeast 2-hybrid and transcriptome analyses, and molecular characterization were performed in this study to uncover the function of the C2orf69 gene. RESULTS. We identified loss-of-function mutations in the uncharacterized C2orf69 gene in 8 individuals with brain abnormalities involving hypomyelination and microcephaly, liver dysfunction, and recurrent autoinflammation. C2orf69 contains an N-terminal signal peptide that is required and sufficient for mitochondrial…

0301 basic medicineMicrocephalyRespiratory chainBiologyMitochondrionCell LineMitochondrial ProteinsTranscriptomeMiceOpen Reading Frames03 medical and health sciencesAll institutes and research themes of the Radboud University Medical Center0302 clinical medicineLoss of Function MutationGlycogen branching enzymemedicineAnimalsHumansGeneMice KnockoutGeneticsMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Glycogen Debranching Enzyme SystemGeneral Medicinemedicine.diseaseMitochondriaOpen reading frameRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]030104 developmental biology030220 oncology & carcinogenesisMicrocephalybiology.proteinClinical MedicineSignal transductionGlycogenJournal of Clinical Investigation
researchProduct

Mitochondria during sea urchin oogenesis.

2017

SummarySea urchin represents an ideal model for studies on fertilization and early development, but the achievement of egg competence and mitochondrial behaviour during oogenesis remain to be enlightened. Oocytes of echinoid, such as sea urchin, unlike other echinoderms and other systems, complete meiotic maturation before fertilization. Mitochondria, the powerhouse of eukaryotic cells, contain a multi-copy of the maternally inherited genome, and are involved directly at several levels in the reproductive processes, as their functional status influences the quality of oocytes and contributes to fertilization and embryogenesis. In the present paper, we report our latest data on mitochondrial…

0301 basic medicineMitochondrial DNAEmbryo NonmammalianMitoTrackerHsp56MitochondrionOogenesisDNA MitochondrialParacentrotus lividusOxidative PhosphorylationTacrolimus Binding Proteins03 medical and health sciencesOogenesisMeiosisbiology.animalPicoGreenAnimalsConfocal laser scanning microscopySettore BIO/06 - Anatomia Comparata E CitologiaSea urchinGerminal vesiclebiologymtDNAAnatomyCell Biologybiology.organism_classificationCell biologyMitochondria030104 developmental biologySea UrchinsOocytesFemaleDevelopmental biologyDevelopmental BiologyZygote (Cambridge, England)
researchProduct

Re-definition and supporting evidence toward Fanconi Anemia as a mitochondrial disease: Prospects for new design in clinical management

2021

Fanconi anemia (FA) has been investigated since early studies based on two definitions, namely defective DNA repair and proinflammatory condition. The former definition has built up the grounds for FA diagnosis as excess sensitivity of patients' cells to xenobiotics as diepoxybutane and mitomycin C, resulting in typical chromosomal abnormalities. Another line of studies has related FA phenotype to a prooxidant state, as detected by both in vitro and ex vivo studies. The discovery that the FA group G (FANCG) protein is found in mitochondria (Mukhopadhyay et al., 2006) has been followed by an extensive line of studies providing evidence for multiple links between other FA gene products and mi…

0301 basic medicineMitochondrial DNAMitochondrial DiseasesMitomycinMitochondrial diseaseClinical BiochemistryDiepoxybutaneReview ArticleMitochondrionBiologyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFanconi anemiaFANCGmedicineHumansClastogenCarnitinelcsh:QH301-705.5Coenzyme Q10lcsh:R5-920ProteinOrganic ChemistryMitochondrial nutrientProteinsmedicine.diseaseMitochondrial diseaseFanconi AnemiaPhenotypeClastogens030104 developmental biologylcsh:Biology (General)chemistryProoxidant stateCancer researchMitochondrial nutrientsMitochondrial dysfunctionlcsh:Medicine (General)030217 neurology & neurosurgeryHumanmedicine.drugRedox Biology
researchProduct

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
researchProduct