Search results for "MITOCHONDRION"

showing 10 items of 491 documents

Loss of response of carnitine palmitoyltransferase I to okadaic acid in transformed hepatic cells

1998

The specific activity of carnitine palmitoyltransferase I (CPT-I) was similar in mitochondria isolated from rat Fao and human HepG2 hepatoma cells and from rat hepatocytes, but almost twofold higher in permeabilized hepatoma cells than in permeabilized hepatocytes. Short-term exposure to okadaic acid induced a ca. 80% stimulation of CPT-I in hepatocytes, whereas no significant response of the enzyme from hepatoma cells was evident. Thus, the high CPT-I activity displayed by hepatoma cells may be reached by hepatocytes upon challenge to okadaic acid. Reconstitution experiments with purified mitochondrial and cytoskeletal fractions showed that the cytoskeleton of hepatocytes produced a more r…

Carcinoma Hepatocellularendocrine system diseasesMitochondria LiverMitochondrionBiologyBiochemistrychemistry.chemical_compoundLiver Neoplasms ExperimentalOkadaic AcidTumor Cells CulturedmedicineAnimalsHumansheterocyclic compoundsCarnitine O-palmitoyltransferaseCytoskeletonneoplasmsCell Line TransformedPharmacologyCarnitine O-PalmitoyltransferaseLiver NeoplasmsOkadaic aciddigestive system diseasesMitochondriaRatsCell biologyKineticsmedicine.anatomical_structureBiochemistrychemistryCell cultureHepatocyteHepatic stellate cellCarnitine palmitoyltransferase IBiochemical Pharmacology
researchProduct

Down-regulation of OPA1 alters mouse mitochondrial morphology, PTP function, and cardiac adaptation to pressure overload

2012

AIMS: The optic atrophy 1 (OPA1) protein is an essential protein involved in the fusion of the mitochondrial inner membrane. Despite its high level of expression, the role of OPA1 in the heart is largely unknown. We investigated the role of this protein in Opa1(+/-) mice, having a 50% reduction in OPA1 protein expression in cardiac tissue. METHODS AND RESULTS: In mutant mice, cardiac function assessed by echocardiography was not significantly different from that of the Opa1(+/+). Electron and fluorescence microscopy revealed altered morphology of the Opa1(+/-) mice mitochondrial network; unexpectedly, mitochondria were larger with the presence of clusters of fused mitochondria and altered c…

Cardiac function curveendocrine systemPhysiologyAdaptation BiologicalDown-RegulationBiologyMitochondrionMitochondrial Membrane Transport ProteinsPermeabilityGTP PhosphohydrolasesMitochondrial ProteinsMice03 medical and health sciencesMitochondrial membrane transport protein0302 clinical medicinePhysiology (medical)Optic Atrophy Autosomal DominantPressuremedicineAnimalsMyocyteMyocytes CardiacInner mitochondrial membrane030304 developmental biologyMice KnockoutPressure overload0303 health sciencesMitochondrial Permeability Transition Poremedicine.diseaseeye diseasesMitochondriaCell biologyBiochemistryMitochondrial permeability transition poreMitochondrial Membranesbiology.proteinOptic Atrophy 1Cardiology and Cardiovascular Medicine030217 neurology & neurosurgeryCardiovascular Research
researchProduct

Differential responses to docosahexaenoic acid in primary and immortalized cardiac cells

2013

Abstract The importance of dietary polyunsaturated fatty acids (PUFAs) in the reduction of cardiovascular disease has been recognized for many years. Docosahexaenoic acid (22:6n3, DHA) is an n-3 PUFA known to affect numerous biological functions and provide cardioprotection; however, the exact molecular and cellular protective mechanism(s) remain unknown. In contrast, DHA also possesses many anti-tumorgenic properties including suppressing cell growth and inducing apoptosis. In the present study, we investigated the effect of DHA toward H9c2 cells (an immortalized cardiac cell line) and neonatal primary cardiomyocytes (NCM). Cells were treated with 0 μM, 10 μM or 100 μM DHA for upto 48 h. C…

CardioprotectionDocosahexaenoic AcidsbiologyCaspase 3Cell SurvivalInterleukin-6Cell growthCytochrome cBlotting WesternCytochromes cGeneral MedicineMitochondrionToxicologyMitochondria HeartCell LineRatsCell biologyDocosahexaenoic acidApoptosiscardiovascular systembiology.proteinAnimalsMyocytes CardiacViability assayCaspaseToxicology Letters
researchProduct

May the force be with you: Transfer of healthy mitochondria from stem cells to stroke cells

2018

Stroke is a major cause of death and disability in the United States and around the world with limited therapeutic option. Here, we discuss the critical role of mitochondria in stem cell-mediated rescue of stroke brain by highlighting the concept that deleting the mitochondria from stem cells abolishes the cells’ regenerative potency. The application of innovative approaches entailing generation of mitochondria-voided stem cells as well as pharmacological inhibition of mitochondrial function may elucidate the mechanism underlying transfer of healthy mitochondria to ischemic cells, thereby providing key insights in the pathology and treatment of stroke and other brain disorders plagued with…

Cardiorespiratory Medicine and HaematologyMitochondrionRegenerative medicineRats Sprague-Dawley0302 clinical medicineStem Cell Research - Nonembryonic - Humanenergy metabolismStrokeStem CellsBrainCerebral ischemiaMitochondriaStrokeNeurologycellular bioenergeticStem Cell Research - Nonembryonic - Non-HumanStem cellmedicine.symptomCardiology and Cardiovascular Medicine1.1 Normal biological development and functioningClinical SciencesEnergy metabolismregenerative medicineInflammation03 medical and health sciencesUnderpinning researchmedicineAnimalsHumansNeurology & NeurosurgeryAnimalbusiness.industryMechanism (biology)NeurosciencesStem Cell Researchmedicine.diseaseRatsBrain DisordersTransplantationDisease Models AnimalinflammationDisease ModelsCommentarycellular bioenergeticsSprague-DawleyNeurology (clinical)businessNeuroscience030217 neurology & neurosurgerytransplantationJournal of Cerebral Blood Flow & Metabolism
researchProduct

Nuclear-mitochondrial interaction.

2007

The biogenesis of mitochondria depends on the coordinated expression of nuclear and mitochondrial genomes. Consequently, the control of mitochondrial biogenesis and function depends on extremely complex processes requiring a variety of well orchestrated regulatory mechanisms. It is clear that the interplay of transcription factors and coactivators contributes to the expression of both nuclear and mitochondrial respiratory genes. In addition, the regulation of mitochondria biogenesis depends on proteins that, interacting with messenger RNAs for mitochondrial proteins, influence their metabolism and expression. Moreover, a tight regulation of the import and final assembly of mitochondrial pro…

Cell NucleusRNA-binding proteinRNA-binding proteinsCell BiologyCell CommunicationBiologyMitochondrionCell biologyEpigenesis GeneticMitochondriamitochondrial fusionMitochondrial biogenesisNeoplasmsMolecular MedicineAnimalsHumansMitochondrial fissionMolecular BiologyTranscription factorPost-transcriptional regulationBiogenesistranscriptional factorpost-transcriptional regulationTranscription FactorsMitochondrion
researchProduct

Involvement of enniatins-induced cytotoxicity in human HepG2 cells.

2012

Enniatins (ENNs) are mycotoxins found in Fusarium fungi and they appear in nature as mixtures of cyclic depsipeptides. The ability to form ionophores in the cell membrane is related to their cytotoxicity. Changes in ion distribution between inner and outer phases of the mitochondria affect to their metabolism, proton gradient, and chemiosmotic coupling, so a mitochondrial toxicity analysis of enniatins is highly recommended because they host the homeostasis required for cellular survival. Two ENNs, ENN A and ENN B on hepatocarcinoma cells (HepG2) at 1.5 and 3 μM and three exposure times (24, 48 and 72 h) were studied. Flow cytometry was used to examine their effects on cell proliferation, t…

Cell SurvivalApoptosisMitochondrionBiologyToxicologyFlow cytometryCell membraneFusariumDepsipeptidesmedicineCytotoxic T cellHumansCytotoxicityCell ProliferationMembrane Potential Mitochondrialmedicine.diagnostic_testCell growthCell CycleGeneral MedicineHep G2 CellsCell cycleMycotoxinsCell biologyMitochondriamedicine.anatomical_structureApoptosisCell DivisionPropidiumToxicology letters
researchProduct

Cytotoxicity of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide in multidrug-resistant cancer cells through activation of PERK/eIF2α/AT…

2021

After decades of research, multidrug resistance (MDR) remains a huge challenge in cancer treatment. In this study, the cytotoxic of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide (MCC1734) has been investigated towards multidrug-resistant cancer cell lines. MCC1734 exerted cytotoxicity on cell lines expressing different mechanisms of drug resistance (P-glycoprotein, BCRP, ABCB5, EGFR, p53 knockout) to a different extent. Interestingly, sensitive CCRF-CEM cells and multidrug-resistant P-gp-overexpressing CEM/ADR5000 cells represented similar sensitivity towards MCC1734, indicating MCC1734 can bypass P-gp-mediated resistance. Microarray-based mRNA expression revealed that MCC17…

Cell SurvivalEukaryotic Initiation Factor-2Antineoplastic AgentsMitochondrionBiochemistryFlow cytometryeIF-2 KinaseCell Line TumorOxazinesmedicineHumansCytotoxic T cellGene Regulatory NetworksCytotoxicityPharmacologyMolecular Structuremedicine.diagnostic_testChemistryCell cycleActivating Transcription Factor 4Gene Expression Regulation NeoplasticXanthenesDrug Resistance NeoplasmCell cultureApoptosisCancer cellCancer researchGene DeletionBiochemical Pharmacology
researchProduct

Profilin 1 is essential for retention and metabolism of mouse hematopoietic stem cells in bone marrow

2014

How stem cells interact with the microenvironment to regulate their cell fates and metabolism is largely unknown. Here we demonstrated that the deletion of the cytoskeleton-modulating protein profilin 1 (pfn1) in hematopoietic stem cell (HSCs) led to bone marrow failure, loss of quiescence, and mobilization and apoptosis of HSCs in vivo. A switch from glycolysis to mitochondrial respiration with increased reactive oxygen species (ROS) level was also observed in HSCs on pfn1 deletion. Importantly, treatment of pfn1-deficient mice with the antioxidant N-acetyl-l-cysteine reversed the ROS level and loss of quiescence of HSCs, suggesting that the metabolism is mechanistically linked to the cell…

Cell SurvivalHematopoiesis and Stem CellsImmunologyCellMice TransgenicMitochondrionBiologyBiochemistryMiceProfilinsBone MarrowCell MovementmedicineAnimalsStem Cell NicheCells CulturedHematopoietic Stem Cell MobilizationHematopoietic stem cellCell BiologyHematologyCell cycleHematopoietic Stem CellsHematopoietic Stem Cell MobilizationCell biologyMice Inbred C57BLHaematopoiesismedicine.anatomical_structureBiochemistryBone marrowStem cellCèl·lules mareGlycolysisProteïnesBlood
researchProduct

Geldanamycin-induced osteosarcoma cell death is associated with hyperacetylation and loss of mitochondrial pool of heat shock protein 60 (hsp60)

2013

Osteosarcoma is one of the most malignant tumors of childhood and adolescence that is often resistant to standard chemo- and radio-therapy. Geldanamycin and geldanamycin analogs have been recently studied as potential anticancer agents for osteosarcoma treatment. Here, for the first time, we have presented novel anticancer mechanisms of geldanamycin biological activity. Moreover, we demonstrated an association between the effects of geldanamycin on the major heat shock proteins (HSPs) and the overall survival of highly metastatic human osteosarcoma 143B cells. We demonstrated that the treatment of 143B cells with geldanamycin caused a subsequent upregulation of cytoplasmic Hsp90 and Hsp70 w…

Cell SurvivalLactams Macrocycliclcsh:MedicineApoptosisBone NeoplasmsBiologyMitochondrionMitochondrial Proteinschemistry.chemical_compoundGeldanamycin Hsp60 Osteosarcoma cellHeat shock proteinCell Line Tumorpolycyclic compoundsBenzoquinonesHumansHeat shocklcsh:ScienceCell ProliferationOsteosarcomaMultidisciplinaryAntibiotics Antineoplasticlcsh:RAcetylationChaperonin 60GeldanamycinHsp90Molecular biologyMitochondriaProtein TransportchemistryCancer cellCancer researchbiology.proteinApoptotic signaling pathwayHSP60lcsh:QDrug Screening Assays AntitumorProtein Processing Post-TranslationalResearch ArticleSignal Transduction
researchProduct

Down-regulation of nuclear binding activities of OXBOX-REBOX transcription factors during cellular senescence.

1996

Functional capacity of mitochondria declines during aging and this impairment may have a major role in aging process. Several observations indicate that transcriptional efficiency is reduced during aging. Our purpose was to find out whether aging and cellular senescence affect the nuclear binding activities of transcription factors which bind to OXBOX-REBOX sequence present in promoter regions of numerous nuclear genes encoding mitochondrial proteins. These factors regulate and coordinate the expression of mitochondrial proteins. We observed a strong down-regulation in the nuclear binding activities of OXBOX-REBOX factors in replicatively senesced human WI-38 and IMR-90 fibroblasts. On the …

Cell cycle checkpointNuclear genePhotoagingMolecular Sequence DataBiophysicsDown-RegulationPlasma protein bindingBiologyMitochondrionBiochemistryDownregulation and upregulationmedicineAnimalsHumansRats WistarMolecular BiologyTranscription factorCellular SenescenceCell Line TransformedBase SequenceNuclear ProteinsCell BiologyDNAmedicine.diseaseCell biologyRatsCell cultureProtein BindingTranscription FactorsBiochemical and biophysical research communications
researchProduct