Search results for "Mito"

showing 10 items of 2513 documents

Does Metformin Protect Diabetic Patients from Oxidative Stress and Leukocyte-Endothelium Interactions?

2017

Since metformin can exert beneficial vascular effects, we aimed at studying its effect on reactive oxygen species (ROS) production, antioxidant enzyme expression, levels of adhesion molecules, and leukocyte-endothelium interactions in the leukocytes from type 2 diabetic (T2D) patients. The study was carried out in 72 T2D patients (41 of whom were treated with metformin for at least 12 months at a dose of 1700 mg per day), and in 40 sex- and age-matched control subjects. Leukocytes from T2D patients exhibited enhanced levels of mitochondrial ROS and decreased mRNA levels of glutathione peroxidase 1 (gpx1) and sirtuin 3 (sirt3) with respect to controls, whereas metformin was shown to revert t…

0301 basic medicineMitochondrial ROSMaleGPX1endocrine system diseasesPhysiologyClinical Biochemistry030204 cardiovascular system & hematologymedicine.disease_causeBiochemistry0302 clinical medicineSuperoxide Dismutase-1Glutathione Peroxidase GPX1Sirtuin 3LeukocytesGeneral Environmental Sciencechemistry.chemical_classificationbiologyMiddle AgedCatalaseIntercellular Adhesion Molecule-1MetforminMetforminP-SelectinCatalaseFemalemedicine.drugmedicine.medical_specialtySIRT3Superoxide dismutase03 medical and health sciencesInternal medicinemedicineCell AdhesionHumansHypoglycemic AgentsMolecular BiologyAgedReactive oxygen speciesGlutathione Peroxidasenutritional and metabolic diseasesEndothelial CellsCell BiologyOxidative Stress030104 developmental biologyEndocrinologychemistryDiabetes Mellitus Type 2biology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidantsredox signaling
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Revisiting the Warburg effect: historical dogma versus current understanding

2020

Contrary to Warburg's original thesis, accelerated aerobic glycolysis is not a primary, permanent and universal consequence of dysfunctional or impaired mitochondria compensating for poor ATP yield per mole of glucose. Instead, in most tumours the Warburg effect is an essential part of a 'selfish' metabolic reprogramming, which results from the interplay between (normoxic/hypoxic) hypoxia-inducible factor-1 (HIF-1) overexpression, oncogene activation (cMyc, Ras), loss of function of tumour suppressors (mutant p53, mutant phosphatase and tensin homologue (PTEN), microRNAs and sirtuins with suppressor functions), activated (PI3K-Akt-mTORC1, Ras-Raf-MEK-ERK-cMyc, Jak-Stat3) or deactivated (LKB…

0301 basic medicineMitochondrial ROSPhysiologyCellular respirationChemistryMitochondrionWarburg effectCell biologyddc:Citric acid cycle03 medical and health sciencesPhosphatidylinositol 3-Kinases030104 developmental biology0302 clinical medicineGlucoseMitochondrial biogenesisAnaerobic glycolysisNeoplasmsTumor MicroenvironmentHumansGlycolysisGlycolysis030217 neurology & neurosurgery
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Insulin Resistance in PCOS Patients Enhances Oxidative Stress and Leukocyte Adhesion: Role of Myeloperoxidase

2016

Cardiovascular diseases and oxidative stress are related to polycystic ovary syndrome (PCOS) and insulin resistance (IR). We have evaluated the relationship between myeloperoxidase (MPO) and leukocyte activation in PCOS patients according to homeostatic model assessment of IR (HOMA-IR), and have explored a possible correlation between these factors and endocrine and inflammatory parameters. This was a prospective controlled study conducted in an academic medical center. The study population consisted of 101 PCOS subjects and 105 control subjects. We divided PCOS subjects into PCOS non-IR (HOMA-IR2.5). Metabolic and anthropometric parameters, total and mitochondrial reactive oxygen species (…

0301 basic medicineMitochondrial ROSendocrine system diseasesmedicine.medical_treatment030204 cardiovascular system & hematologyPathology and Laboratory Medicinemedicine.disease_causeBiochemistryWhite Blood CellsFluorescence MicroscopyEndocrinology0302 clinical medicineAnimal CellsMedicine and Health SciencesLeukocytesInsulinImmune ResponseEnergy-Producing OrganellesMicroscopyMultidisciplinaryQRLight MicroscopyPolycystic ovaryMitochondriaOncologyMyeloperoxidaseHomeostatic model assessmentCytokinesMedicineFemaleCellular TypesCellular Structures and OrganellesInflammation MediatorsResearch ArticlePolycystic Ovary SyndromeAdultmedicine.medical_specialtyAdhesion MoleculesImmune CellsScienceImmunologyBioenergeticsBiologyResearch and Analysis MethodsProinflammatory cytokineYoung Adult03 medical and health sciencesSigns and SymptomsInsulin resistanceDiagnostic MedicineInternal medicineCell AdhesionmedicineHumansPeroxidaseInflammationDiabetic EndocrinologyBlood CellsInsulinBiology and Life SciencesCancers and Neoplasmsnutritional and metabolic diseasesCell BiologyMolecular Developmentmedicine.diseaseHormonesOxidative Stress030104 developmental biologyEndocrinologybiology.proteinInsulin ResistanceReactive Oxygen SpeciesGynecological TumorsOxidative stressDevelopmental Biology
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Ribosome-Targeting Antibiotics Impair T Cell Effector Function and Ameliorate Autoimmunity by Blocking Mitochondrial Protein Synthesis

2019

Summary While antibiotics are intended to specifically target bacteria, most are known to affect host cell physiology. In addition, some antibiotic classes are reported as immunosuppressive for reasons that remain unclear. Here, we show that Linezolid, a ribosomal-targeting antibiotic (RAbo), effectively blocked the course of a T cell-mediated autoimmune disease. Linezolid and other RAbos were strong inhibitors of T helper-17 cell effector function in vitro, showing that this effect was independent of their antibiotic activity. Perturbing mitochondrial translation in differentiating T cells, either with RAbos or through the inhibition of mitochondrial elongation factor G1 (mEF-G1) progressi…

0301 basic medicineMitochondrial translationmedicine.medical_treatmentT-LymphocytesCellMitochondrionmedicine.disease_causeRibosomemitochondrial translationOxidative PhosphorylationantibioticsAutoimmunityACTIVATIONMice0302 clinical medicineribosome-targetingMedicine and Health SciencesImmunology and AllergyTRANSCRIPTION FACTORMolecular Targeted TherapyMice Knockout0303 health sciencesEffectorExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationPeptide Elongation Factor GAnti-Bacterial Agents3. Good healthCell biologymitochondriaInfectious DiseasesCytokinemedicine.anatomical_structureRESPIRATION030220 oncology & carcinogenesisEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisT cellImmunologyINHIBITIONT cellsBiologyOXAZOLIDINONEPeptides CyclicArticleMitochondrial Proteins03 medical and health sciencesNAD+medicineAnimalsHumanselongation factor G1030304 developmental biologyAutoimmune diseaseBacteriaLinezolidBiology and Life SciencesPATHWAYSDNANADmedicine.diseaseIn vitroMice Inbred C57BL030104 developmental biologyTh17 CellsArgyrinCHLORAMPHENICOLMEMBRANERibosomesImmunity
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Stem Cell-Derived, microRNA-Carrying Extracellular Vesicles: A Novel Approach to Interfering with Mesangial Cell Collagen Production in a Hyperglycae…

2016

Extracellular vesicles (EVs) that are derived from stem cells are proving to be promising therapeutic options. We herein investigate the therapeutic potential of EVs that have been derived from different stem cell sources, bone-marrow (MSC) and human liver (HLSC), on mesangial cells (MCs) exposed to hyperglycaemia. By expressing a dominant negative STAT5 construct (ΔNSTAT5) in HG-cultured MCs, we have demonstrated that miR-21 expression is under the control of STAT5, which translates into Transforming Growth Factor beta (TGFβ) expression and collagen production. A number of approaches have been used to show that both MSC- and HLSC-derived EVs protect MCs from HG-induced damage via the trans…

0301 basic medicineMolecular biologyCellGene Expressionlcsh:MedicineBiochemistry0302 clinical medicineAnimal CellsChronic Kidney DiseaseMedicine and Health SciencesSTAT5 Transcription FactorRNA Processing Post-Transcriptionallcsh:ScienceSTAT5Energy-Producing OrganellesCells CulturedMultidisciplinarybiologyMesangial cellStem CellsVector ConstructionCell biologyMitochondriaEnzymesmedicine.anatomical_structureBiochemistryNephrology030220 oncology & carcinogenesisMesangial CellsCollagenStem cellCellular TypesCellular Structures and OrganellesOxidoreductasesLuciferaseResearch ArticleCollagen Type IVBioenergeticsDNA constructionModels Biological03 medical and health sciencesExtracellular VesiclesmicroRNAmedicineGene Expression and Vector TechniquesGeneticsHumansVesiclesCell ProliferationMolecular Biology Assays and Analysis TechniquesCell growthMesenchymal stem celllcsh:RBiology and Life SciencesProteinsMesenchymal Stem CellsTransforming growth factor betaCell BiologyResearch and analysis methodsMicroRNAs030104 developmental biologyMolecular biology techniquesGlucoseHyperglycemiabiology.proteinEnzymologylcsh:QCollagensPLoS ONE
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Bax transmembrane domain interacts with prosurvival Bcl-2 proteins in biological membranes

2016

The Bcl-2 (B-cell lymphoma 2) protein Bax (Bcl-2 associated X, apoptosis regulator) can commit cells to apoptosis via outer mitochondrial membrane permeabilization. Bax activity is controlled in healthy cells by prosurvival Bcl-2 proteins. C-terminal Bax transmembrane domain interactions were implicated recently in Bax pore formation. Here, we show that the isolated transmembrane domains of Bax, Bcl-xL (B-cell lymphoma-extra large), and Bcl-2 can mediate interactions between Bax and prosurvival proteins inside the membrane in the absence of apoptotic stimuli. Bcl-2 protein transmembrane domains specifically homooligomerize and heterooligomerize in bacterial and mitochondrial membranes. Thei…

0301 basic medicineMultidisciplinary030102 biochemistry & molecular biologyChemistryApoptosis RegulatorapoptosisBiological membraneBiological SciencesBioinformaticsBiotecnologiaOuter mitochondrial membraneoligomerizationtransmembraneCell biologymitochondria03 medical and health sciencesTransmembrane domain030104 developmental biologyMembraneMembranes (Biologia)ApoptosisBcl-2ProteïnesProceedings of the National Academy of Sciences
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Cytotoxicity of 18 Cameroonian medicinal plants against drug sensitive and multi-factorial drug resistant cancer cells

2018

Abstract Ethnopharmacological relevance Cameroonian medicinal plants are traditionally used to treat many ailments, including cancer and related diseases. Cancer is characterized as a condition with complex signs and symptoms. It has been recommended that ethnopharmacological usages such as immune and skin disorders, inflammatory, infectious, parasitic and viral diseases should be taken into account when selecting plants for anticancer screenings, since these reflect disease states bearing relevance to cancer or cancer-like symptoms. Aim of the study The present study aims at investigating 20 methanol extracts from 15 Cameroonian medicinal plants on a panel of human cancer cell lines, inclu…

0301 basic medicineNaucleaCell SurvivalAntineoplastic AgentsApoptosisMagnoliopsida03 medical and health sciencesPhytomedicine0302 clinical medicineMorus mesozygiaCell Line TumorDrug DiscoverymedicineHumansCameroonMedicinal plantsErythrinaMembrane Potential MitochondrialPharmacologyPlants MedicinalbiologyTraditional medicinePlant ExtractsCancerbiology.organism_classificationmedicine.diseaseDrug Resistance Multiple030104 developmental biologyDrug Resistance NeoplasmCaspases030220 oncology & carcinogenesisvisual_artCancer cellvisual_art.visual_art_mediumBarkReactive Oxygen SpeciesJournal of Ethnopharmacology
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Levosimendan protects human hepatocytes from ischemia-reperfusion injury.

2017

Background Ischemia-reperfusion injury (IRI) is a major challenge in liver transplantation. The mitochondrial pathway plays a pivotal role in hepatic IRI. Levosimendan, a calcium channel sensitizer, was shown to attenuate apoptosis after IRI in animal livers. The aim of this study was to investigate the effect of levosimendan on apoptosis in human hepatocytes. Methods Primary human hepatocytes were either exposed to hypoxia or cultured under normoxic conditions. After the hypoxic phase, reoxygenation was implemented and cells were treated with different concentrations of levosimendan (10ng/ml, 100ng/ml, 1000ng/ml). The overall metabolic activity of the cells was measured using 3-(4,5-dimeth…

0301 basic medicineNecrosisCritical Care and Emergency Medicinelcsh:MedicineApoptosis030204 cardiovascular system & hematologyBiochemistry0302 clinical medicineAnimal CellsMedicine and Health SciencesEnzyme assaysColorimetric assayslcsh:ScienceBioassays and physiological analysisCells CulturedEnergy-Producing Organellesbcl-2-Associated X ProteinMultidisciplinaryMTT assaybiologyCell DeathMitochondriaPyridazinesLiverCell ProcessesReperfusion Injurymedicine.symptomCellular TypesAnatomyCellular Structures and Organellesmedicine.drugResearch Articlemedicine.medical_specialtyCell PhysiologyIschemiaCardiologySurgical and Invasive Medical ProceduresBioenergetics03 medical and health sciencesDigestive System ProceduresBcl-2-associated X proteinInternal medicinemedicineHumansMTT assayddc:610SimendanHeart FailureTransplantationbusiness.industrylcsh:RHydrazonesBiology and Life SciencesLevosimendanCell BiologyOrgan TransplantationHypoxia (medical)medicine.diseaseLiver TransplantationCell MetabolismResearch and analysis methods030104 developmental biologyEndocrinologyApoptosisReperfusionBiochemical analysisbiology.proteinHepatocyteslcsh:QbusinessReperfusion injuryPloS one
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Effects of acetyl-l-carnitine in diabetic neuropathy and other geriatric disorders

2018

A long history of diabetes mellitus and increasing age are associated with the onset of diabetic neuropathy, a painful and highly disabling complication with a prevalence peaking at 50% among elderly diabetic patients. Acetyl-l-carnitine (ALC) is a molecule derived from the acetylation of carnitine in the mitochondria that has an essential role in energy production. It has recently been proposed as a therapy to improve the symptoms of diabetic neuropathy. ALC is widely distributed in mammalian tissues, including the brain, blood–brain barrier, brain neurons, and astrocytes. Aside from its metabolic activity, ALC has demonstrated cytoprotective, antioxidant, and antiapoptotic effects in the …

0301 basic medicineNervous systemAgingmedicine.medical_specialtyDiabetic neuropathyDiabetic neuropathyPainNeurotrophic effectAcetyl-l-carnitine; Analgesia; Diabetic neuropathy; Neurotrophic effect; Aging; Geriatrics and GerontologyNO03 medical and health sciences0302 clinical medicineDiabetic NeuropathiesAlzheimer DiseaseInternal medicineDiabetes mellitusmedicineHumansCarnitineAcetyl-l-carnitine; Analgesia; Diabetic neuropathy; Neurotrophic effectAcetylcarnitineAcetyl-l-carnitine Diabetic neuropathy Analgesia Neurotrophic effectAgedAnalgesicsbusiness.industryGlutamate receptormedicine.diseaseMitochondriaAcetyl-l-carnitine030104 developmental biologyNerve growth factorEndocrinologymedicine.anatomical_structureAnalgesiaGeriatrics and GerontologyAlzheimer's diseaseAcetylcarnitinebusiness030217 neurology & neurosurgerymedicine.drug
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