Search results for "mitochondrial"

showing 10 items of 919 documents

Effect of an Ilex paraguariensis (yerba mate) extract on infarct size in isolated rat hearts: the mechanisms involved

2016

Tea made from Ilex paraguariensis (IP) dried and minced leaves is a beverage widely consumed by large populations in South America as a source of caffeine (stimulant action) and for its medicinal properties. However, there is little information about the action of IP on the myocardium in the ischemia-reperfusion condition. Therefore, the objective of this study was to examine the effects of an aqueous extract of IP on infarct size in a model of regional ischemia. Isolated rat hearts were perfused by the Langendorff technique and subjected to 40 min of coronary artery occlusion followed by 60 min of reperfusion (ischemic control hearts). Other hearts received IP 30 μg mL-1 during the first 1…

0301 basic medicineMaleCIENCIAS MÉDICAS Y DE LA SALUDThiobarbituric acidIschemiaInmunologíaMyocardial InfarctionPharmacologyIn Vitro TechniquesIlex Paraguariensis03 medical and health scienceschemistry.chemical_compoundfoodIlex paraguariensisYerba-mateTBARSMedicineAnimalsHumansRats WistarIschemia-Reperfusionbiologybusiness.industryPlant ExtractsMyocardiumHeartGeneral MedicineGlutathione//purl.org/becyt/ford/3.1 [https]medicine.diseaseGlutathionefood.foodRatsNitric oxide synthaseMedicina Básica030104 developmental biologyMitochondrial permeability transition poreBiochemistrychemistrybiology.protein//purl.org/becyt/ford/3 [https]Nitric Oxide SynthasebusinessCaffeineFood Science
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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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
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Sex-based differences after a single bout of exercise on PGC1α isoforms in skeletal muscle: A pilot study

2020

To date, there are limited and incomplete data on possible sex-based differences in fiber-types of skeletal muscle and their response to physical exercise. Adult healthy male and female mice completed a single bout of endurance exercise to examine the sex-based differences of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), heat shock protein 60 (Hsp60), interleukin 6 (IL-6) expression, as well as the Myosin Heavy Chain (MHC) fiber-type distribution in soleus and extensor digitorum longus (EDL) muscles. Our results showed for the first time that in male soleus, a muscle rich of type IIa fibers, endurance exercise activates specifically genes involved in mito…

0301 basic medicineMalemedicine.medical_specialtyAlpha (ethology)interleukin 6Physical exerciseMotor ActivityBiochemistryMitochondrial Proteins03 medical and health sciencesMice0302 clinical medicineSex FactorsEndurance trainingphysical exerciseInternal medicineHeat shock proteinMyosinGeneticsmedicineAnimalsProtein Isoformsskeletal muscleInterleukin 6Muscle SkeletalMolecular BiologyMice Inbred BALB Cbiologybusiness.industryInterleukin-6Myosin Heavy ChainSkeletal muscleChaperonin 60musculoskeletal systemPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha030104 developmental biologyEndocrinologymedicine.anatomical_structureMitochondrial biogenesisbiology.proteinFemalebusiness030217 neurology & neurosurgeryheat shock protein 60Biotechnology
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Mitochondrial genetic haplogroups and depressive symptoms: A large study among people in North America.

2017

Background:\ud A possible relationship between mitochondrial haplogroups and psychiatric diseases (e.g. schizophrenia and bipolar disorder) has been postulated, but data regarding depression is still limited. We investigated whether any mitochondrial haplogroup carried a significant higher risk of depressive symptoms in a large prospective cohort of North American people included in the Osteoarthritis Initiative.\ud \ud Methods:\ud Cross sectional data was derived from the Osteoarthritis Initiative. The haplogroup was assigned through a combination of sequencing and PCR-RFLP techniques. All the mitochondrial haplogroups were named following this nomenclature: H, U, K, J, T, V, SuperHV, I, W…

0301 basic medicineMalemitochondrial haplogroupsCross-sectional studyHaplogroup H*Osteoarthritis initiativePopulation*Mitochondrial haplogroupsDNA MitochondrialHaplogroupArticleWhite People03 medical and health sciences0302 clinical medicineMedicineHumansGenetic Predisposition to DiseaseBipolar disorderProspective Studieseducationeducation.field_of_studybusiness.industryDepressionHaplotypeOsteoarthritis initiativeMiddle Agedmedicine.disease*Depressionhumanities3. Good healthDepression; Mitochondrial haplogroups; Osteoarthritis initiative; Clinical Psychology; Psychiatry and Mental HealthClinical PsychologyMitochondrial haplogroups Depression Osteoarthritis initiative030104 developmental biologyMoodCross-Sectional StudiesHaplotypesPsychiatry and Mental HealthNorth AmericadepressionMitochondrial haplogroupsFemalebusinessosteoarthritis initiative030217 neurology & neurosurgeryHuman mitochondrial DNA haplogroupDemographyClinical psychology
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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
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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
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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
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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
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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)
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