Search results for " mito."

showing 10 items of 892 documents

Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardioto…

2015

Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal model…

Cardiac function curveACE inhibitorsCardiotonic AgentsNeuregulin-1CardiomyopathyAntineoplastic AgentsPreclinical modelsCardioprotectionCardiotonic AgentsPharmacologyBioinformaticsmedicine.disease_causeCancer therapy-induced cardiac injury ;Preclinical modelsMitochondria HeartBeta-blockersNeoplasmsCancer therapy-induced cardiac injuryMedicineAnimalsHumansCardiac stem cellsCardioprotectionCardiotoxicityACE inhibitors; Beta-blockers; Cancer therapy-induced cardiac injury; Cardiac stem cells; Cardioprotection; Mitochondria; Neuregulin-1; Oxidative stress; Preclinical models; Statinsbusiness.industryStatinsCancermedicine.diseaseCardiotoxicityMitochondriaCancer therapy-induced cardiac injury Preclinical models Cardioprotection Mitochondria Neuregulin-1 Oxidative stress Statins Beta-blockers ACE inhibitors Cardiac stem cellsDisease Models AnimalOxidative StressHeart failureCardiology and Cardiovascular MedicinebusinessOxidative stress
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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
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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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Transcriptional and post-transcriptional regulation of iNOS expression in human chondrocytes

2009

Chondrocytes are important for the development and maintenance of articular cartilage. However, both in osteoarthritis (OA) and rheumatoid arthritis (RA) chondrocytes are involved in the process of cartilage degradation and synthesize important immunomodulatory mediators, including nitric oxide (NO) generated by the inducible NO synthase (iNOS). To uncover the role of iNOS in the pathomechanisms of OA and RA, we analyzed the regulation of iNOS expression using immortalized human chondrocytes as a reproducible model. In C-28/I2 chondrocytes, iNOS expression was associated with the expression of the chondrocyte phenotype. Peak induction by a cytokine cocktail occurred between 6 and 8h and dec…

Cartilage Articularmedicine.medical_specialtyAnti-Inflammatory AgentsNitric Oxide Synthase Type IIBiologyBiochemistryp38 Mitogen-Activated Protein KinasesChondrocyteArticleGene Expression Regulation EnzymologicGlucocorticoid receptorChondrocytesReceptors GlucocorticoidInternal medicineGene expressionmedicineHumansRNA MessengerRNA Processing Post-TranscriptionalPost-transcriptional regulationCell Line TransformedPharmacologyRegulation of gene expressionNF-kappa B p50 SubunitRNA-Binding ProteinsInterferon-Stimulated Gene Factor 3Janus Kinase 2Cell biologyNitric oxide synthaseEndocrinologymedicine.anatomical_structureCell cultureEnzyme Inductionbiology.proteinTrans-ActivatorsCytokinesZearalenoneSignal transduction
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Cigarette Smoke Extract Induces p38 MAPK-Initiated, Fas-Mediated Eryptosis

2022

Eryptosis is a physiological mechanism for the clearance of senescent or damaged erythrocytes by phagocytes. Excessive eryptosis is stimulated under several pathologies and associated with endothelial injury and thrombosis. Cigarette smoke (CS) is an established risk factor for vascular diseases and cigarette smokers have high-levels of eryptotic erythrocytes. This study, for the first time, investigates the mechanism by which CS damages red blood cells (RBCs). CS extract (CSE) from commercial cigarettes was prepared and standardized for nicotine content. Cytofluorimetric analysis demonstrated that treatment of human RBCs with CSE caused dose-dependent, phosphatidylserine externalization an…

Caspase 8ErythrocytesCaspase 3cigarette smokeOrganic ChemistryGeneral Medicinep38 MAPKCeramidesp38 Mitogen-Activated Protein KinasesCatalysisComputer Science ApplicationsInorganic Chemistryeryptosis; cigarette smoke; death-inducing signaling complex (DISC); p38 MAPK; ceramide; caspasescaspasesSmokeeryptosisSettore BIO/10 - BiochimicaTobaccodeath-inducing signaling complex (DISC)HumansceramidePhysical and Theoretical ChemistryReactive Oxygen SpeciesMolecular BiologySpectroscopy
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Temporal speciation pattern in the western Mediterranean genus Tudorella P. Fischer, 1885 (Gastropoda, Pomatiidae) supports the Tyrrhenian vicariance…

2009

The land snail genus Tudorella shows a peculiar disjunct distribution around the western Mediterranean coasts. Despite high phenotypic plasticity, only two species with a disputed number of subspecific taxa are currently recognised. We delimited the species with mitochondrial (COI & 16S) and nuclear (ITS-1) markers based on the unified species concept and suggested that there are eight species in the genus, two of them currently undescribed. Applying Bayesian phylogenetic model selection, we tested four different biogeographic hypotheses that could be causal for the current distribution pattern of extant Tudorella species. A scenario involving vicariance events resulting from the repeated s…

Cell NucleusPhylogenetic treeGeographyModels GeneticLand bridgeEcologyGenetic SpeciationMediterranean RegionSnailsDisjunct distributionLand snailBayes TheoremSequence Analysis DNABiologyDNA MitochondrialEvolution MolecularTaxonGenusGeneticsVicarianceBiological dispersalAnimalsMolecular BiologyEcology Evolution Behavior and SystematicsPhylogenyMolecular phylogenetics and evolution
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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
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Hsp60 is actively secreted by human tumor cells

2010

Background Hsp60, a Group I mitochondrial chaperonin, is classically considered an intracellular chaperone with residence in the mitochondria; nonetheless, in the last few years it has been found extracellularly as well as in the cell membrane. Important questions remain pertaining to extracellular Hsp60 such as how generalized is its occurrence outside cells, what are its extracellular functions and the translocation mechanisms that transport the chaperone outside of the cell. These questions are particularly relevant for cancer biology since it is believed that extracellular chaperones, like Hsp70, may play an active role in tumor growth and dissemination. Methodology/Principal Findings S…

Cell SurvivalBlotting WesternCellImmunology/Immunomodulationlcsh:MedicineApoptosisBiologyExosomesCell LineAmilorideCell membraneMicroscopy Electron TransmissionCell Line TumorNeoplasmsBiochemistry/Cell Signaling and Trafficking StructuresExtracellularmedicineHumansSecretionlcsh:ScienceMultidisciplinarySettore BIO/16 - Anatomia Umanabeta-Cyclodextrinslcsh:RChaperonin 60MicrovesiclesCell biologyPathology/PathophysiologyHSP60 Mitochondria Chaperonopatiesmedicine.anatomical_structureCell cultureCulture Media ConditionedCancer cellAcetylcholinesteraselcsh:QExtracellular SpaceK562 CellsIntracellularResearch Article
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Cisplatin sensitivity is related to late DNA damage processing and checkpoint control rather than to the early DNA damage response

2008

The present study aimed at elucidating mechanisms dictating cell death triggered by cisplatin-induced DNA damage. We show that CL-V5B hamster mutant cells, a derivative of V79B, are hypersensitive to cisplatin-induced apoptotic death. CL-V5B cells are characterized by attenuated cisplatin-induced early (2-6 h) stress response, such as phosphorylation of stress-activated protein kinases (SAPK/JNK), ATM and Rad3-related (ATR) protein kinase, histone H2AX and checkpoint kinase-1 (Chk-1). Human FANCC cells also showed a reduced phosphorylation of H2AX and SAPK/JNK at early time point after cisplatin treatment. This was not the case for BRCA2-defective VC-8 hamster cells, indicating that the FA …

Cell cycle checkpointCisplatin-DNA adducts ; DNA repair ; Interstrand cross links ; DNA damage response ; Cell cycle checkpoint ; Cell deathDNA damageDNA repairHealth Toxicology and MutagenesisApoptosisCell LineHistonesDNA AdductsCricetinaeGeneticsmedicineAnimalsHumansCHEK1PhosphorylationMolecular BiologyChromosome AberrationsCisplatinbiologyJNK Mitogen-Activated Protein KinasesDNA replicationG2-M DNA damage checkpointMolecular biologyCell biologyHistonebiology.proteinCisplatinDNA DamageMutagensmedicine.drug
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