Search results for " Mito"

showing 10 items of 895 documents

Cytotoxic effects of Jay Amin hydroxamic acid (JAHA), a ferrocene-based class I histone deacetylase inhibitor, on triple-negative MDA-MB231 breast ca…

2012

The histone deacetylase inhibitors (HDACis) are a class of chemically heterogeneous anticancer agents of which suberoylanilide hydroxamic acid (SAHA) is a prototypical member. SAHA derivatives may be obtained by three-dimensional manipulation of SAHA aryl cap, such as the incorporation of a ferrocene unit like that present in Jay Amin hydroxamic acid (JAHA) and homo-JAHA [ Spencer , et al. ( 2011 ) ACS Med. Chem. Lett. 2 , 358 - 362 ]. These metal-based SAHA analogues have been tested for their cytotoxic activity toward triple-negative MDA-MB231 breast cancer cells. The results obtained indicate that of the two compounds tested, only JAHA was prominently active on breast cancer cells with a…

medicine.drug_classCell SurvivalMetallocenesAntineoplastic AgentsApoptosisToxicologyHydroxamic AcidsStructure-Activity RelationshipIn vivoAnnexinmedicineTumor Cells CulturedCytotoxic T cellHumansFerrous CompoundsSettore BIO/06 - Anatomia Comparata E Citologiachemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesDose-Response Relationship DrugMolecular StructureChemistryHistone deacetylase inhibitorCell CycleGeneral MedicineIn vitroHistone Deacetylase InhibitorsBiochemistryhistone deacetylase inhibitor breast cancer autophagy apoptosis mitochondria cell cycleApoptosisCancer researchHistone deacetylaseDrug Screening Assays AntitumorReactive Oxygen Species
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Amphiregulin activates human hepatic stellate cells and is upregulated in non alcoholic steatohepatitis

2015

AbstractAmphiregulin (AR) involvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study. Non-alcoholic fatty liver disease (NAFLD) and its more severe form non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hepatocellular cancer (HCC). Our aim was to investigate ex vivo the effect of AR on human primary HSC (hHSC) and verify in vivo the relevance of AR in NAFLD fibrogenesis. hHSC isolated from healthy liver segments were analyzed for expression of AR and its activator, TNF-α converting enzyme (TACE). AR induction of hHSC proliferation and matrix production was estimated in the presence of antagonists. AR involvement in fibrogenesis was also ass…

medicine.medical_specialtyBiopsyGene ExpressionADAM17 ProteinBiologyAmphiregulinSeverity of Illness Indexp38 Mitogen-Activated Protein Kinasesdigestive systemArticleMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineDownregulation and upregulationAmphiregulinGrowth factor receptorNon-alcoholic Fatty Liver DiseaseInternal medicineHepatic Stellate CellsmedicineAnimalsHumansProtein Kinase CPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesMultidisciplinaryFatty livernutritional and metabolic diseasesmedicine.diseaseFibrosisActinsdigestive system diseases3. Good healthEnzyme ActivationErbB ReceptorsADAM ProteinsDisease Models AnimalEndocrinologyHepatic stellate cellCancer research030211 gastroenterology & hepatologyTumor necrosis factor alphaCollagenSteatohepatitisSignal TransductionScientific Reports
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Dual specificity phosphatase 1 knockout mice show enhanced susceptibility to anaphylaxis but are sensitive to glucocorticoids.

2007

Dual specificity phosphatase DUSP1 (otherwise known as mitogen-activated phosphatase 1 or MKP-1) dephosphorylates MAPKs, particularly p38, and negatively regulates innate immunity. Recent studies have shown that the DUSP1 gene is transcriptionally up-regulated by glucocorticoids (GCs) and that the antiinflammatory action of GCs is impaired in DUSP1-/- mice. Here we show that GC-mediated dephosphorylation of ERK-1 and ERK-2 activated by IgE receptor cross-linking is unimpaired in bone marrow-derived mast cells (BMMCs) of DUSP1-/- mice. Dephosphorylation of phospho-p38 MAPK is impaired but only at early times of GC treatment. Proinflammatory cytokine and chemokine gene expression (CCL2, IL-6,…

medicine.medical_specialtyChemokinePhosphataseImmunoglobulin Ep38 Mitogen-Activated Protein KinasesProinflammatory cytokineDephosphorylationMiceEndocrinologyInternal medicineSepsisDual-specificity phosphatasemedicineAnimalsGenetic Predisposition to DiseaseMolecular BiologyAnaphylaxisGlucocorticoidsMice KnockoutMitogen-Activated Protein Kinase 1Mice Inbred C3HMitogen-Activated Protein Kinase 3biologyInterleukin-6Tumor Necrosis Factor-alphaDegranulationDual Specificity Phosphatase 1General MedicineMice Inbred C57BLEndocrinologyGene Expression RegulationMice Inbred DBAbiology.proteinCytokinesTumor necrosis factor alphaMolecular endocrinology (Baltimore, Md.)
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Aging of the liver: Age-associated mitochondrial damage in intact hepatocytes

1996

Mitochondrial damage may be a major cause of cellular aging. So far, this hypothesis had only been tested using isolated mitochondria. The aim of this study was to investigate the involvement of mitochondria in aging using whole liver cells and not isolated mitochondria only. Using flow cytometry, we found that age is associated with a decrease in mitochondrial membrane potential (30%), an increase in mitochondrial size, and an increase in mitochondrial peroxide generation (23%). Intracellular peroxide levels were also increased. The number of mitochondria per cell and inner mitochondrial membrane mass did not change. Gluconeogenesis from glycerol or fructose (mitochondrial-independent) did…

medicine.medical_specialtyHepatologyMitochondrionBiologyMitochondrial SizePyruvate carboxylaseEndocrinologyMitochondrial permeability transition poreGluconeogenesisInternal medicinemedicinesense organsATP–ADP translocaseInner mitochondrial membranePhosphoenolpyruvate carboxykinaseHepatology
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Cardiovascular comorbidity in multiple sclerosis patients treated with mitoxantrone therapy: a cohort study

2017

Abstract Background Mitoxantrone (MX) has been used as second line therapy for aggressive multiple sclerosis (MS). Potential cardiotoxic effects of MX limit its use; a cumulative dose of up to 100 mg/m2, has been long considered relatively safe. We calculated the frequency of cardiac side effects in MS patients treated with MX. Methods We performed a cohort study including all MS patients treated with MX at the Neurological Department of the University Hospital of Palermo, Italy. Two hundred-sixty-four MS patients diagnosed according to validated criteria were included and followed-up until the end of September 2010. Patients were treated with MX as a second line therapy if they had no prev…

medicine.medical_specialtyImmunologyHeart failureComorbidity030204 cardiovascular system & hematologylcsh:RC346-429Multiple sclerosis03 medical and health sciences0302 clinical medicineInternal medicinemedicineImmunology and AllergyMyocardial infarctionlcsh:Neurology. Diseases of the nervous systemMitoxantroneEjection fractionmedicine.diagnostic_testCumulative dosebusiness.industryComorbidity Multiple sclerosis Heart failure Mitoxantrone Therapymedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareNeurologyHeart failureCohortPhysical therapySettore MED/26 - NeurologiaTherapyNeurology (clinical)MitoxantronebusinessElectrocardiography030217 neurology & neurosurgeryCohort studymedicine.drug
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Neuroendocrine Regulation Of The IL-27-Dependent Immune Response In Macrophages

2013

Abstract The central nervous system has the ability for modulating immune responses, but the molecular mechanisms of such interactions are only partly understood. Interleukin-27 (IL-27) is a heterodimeric protein and structurally related to the IL-12 family of cytokines. IL-27 is composed of the subunits EBI3 and p28. The biological functions of IL-27 have been described as either anti-inflammatory or pro-inflammatory depending on the experimental models studied. In the current study, we investigated how production of Interleukin-27 (IL-27) is regulated by neuroendocrine hormones. We focused our work on the subunit p28, since EBI3 is also present in IL-35 and therefore is not a specific com…

medicine.medical_specialtyLipopolysaccharidebiologyp38 mitogen-activated protein kinasesmedicine.medical_treatmentImmunologyInflammationCell BiologyHematologyBiochemistrychemistry.chemical_compoundEndocrinologyCytokineImmune systemchemistryIntegrin alpha MInternal medicinemedicinebiology.proteinmedicine.symptomReceptorHormoneBlood
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Lysine triggers apoptosis through a NADPH oxidase-dependent mechanism in human renal tubular cells

2012

Progressive chronic kidney disease (CKD) is common in lysinuric protein intolerance (LPI), a primary inherited aminoaciduria characterized by massive Lysine excretion in urine. However, by which mechanisms Lysine may cause kidney damage to tubule cells is still not understood. This study determined whether Lysine overloading of human proximal tubular cells (HK-2) in culture enhances apoptotic cell loss and its associated mechanisms. Overloading HK-2 with Lysine levels reproducing those observed in urine of patients affected by LPI (10 mM) increased apoptosis (+30%; p < 0.01 vs.C), as well as Bax and Apaf-1 expressions (+30-50% p < 0.05), while downregulated Bcl-2 (-40% p < 0.05). Apoptosis …

medicine.medical_specialtyLysineGene ExpressionApoptosisNADPH Oxidasecomplex mixturesAntioxidantsCell LineExcretionKidney Tubules ProximalInternal medicineGeneticsmedicineHumansRenal Insufficiency ChronicAmino Acid Metabolism Inborn ErrorsProtein SubunitGenetics (clinical)Membrane Potential MitochondrialKidneyNADPH oxidasebiologyLysineAmino Acid Metabolism Inborn ErrorNADPH OxidasesApoptosimedicine.diseaseCaspase InhibitorsLysinuric protein intoleranceIn vitroProtein SubunitsEndocrinologymedicine.anatomical_structureCell cultureApoptosisbiology.proteinCaspase InhibitorDisease ProgressionAntioxidantReactive Oxygen SpeciesReactive Oxygen SpecieHuman
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PGC-1α: a master gene that is hard to master

2012

Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a transcriptional coactivator that favorably affects mitochondrial function. This concept is supported by an increasing amount of data including studies in PGC-1α gene-deleted mice, suggesting that PGC-1α is a rescue factor capable of boosting cell metabolism and promoting cell survival. However, this view has now been called into question by a recent study showing that adeno-associated virus-mediated PGC-1α overexpression causes overt cell degeneration in dopaminergic neurons. How is this to be understood, and can these seemingly conflicting findings tell us something about the role of PGC-1α in cell stress and in cont…

medicine.medical_specialtyModels NeurologicalSettore BIO/11 - Biologia MolecolareRNA-binding proteinBiologyMitochondrionSettore BIO/09 - FisiologiaMiceCellular and Molecular NeuroscienceHeat shock proteinInternal medicinemedicineAnimalsHomeostasisHumansReceptorMolecular BiologyTranscription factorHeat-Shock ProteinsMice KnockoutPharmacologyPGC-1α Mitochondria Dopaminergic neurons Transgenic animal Adenovirus Parkinson’s diseaseDopaminergic NeuronsDopaminergicRNA-Binding ProteinsParkinson DiseaseCell BiologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaEndocrinologyCell metabolismNerve DegenerationTrans-ActivatorsMolecular MedicineNeuroscienceHomeostasisTranscription FactorsCellular and Molecular Life Sciences
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Mechanisms of C-reactive protein-induced blood-brain barrier disruption.

2009

Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways. Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation. Results— We could show that CRP at clinically relevant concentrations (10 to 20 μg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fcγ receptors CD16/32 fo…

medicine.medical_specialtyMyosin light-chain kinaseMyosin Light ChainsGuinea PigsBrain Edemamedicine.disease_causeBlood–brain barrierp38 Mitogen-Activated Protein KinasesMyosin light chain kinase activityTight JunctionsInternal medicineMyosinmedicineAnimalsPhosphorylationReceptorCells CulturedAdvanced and Specialized Nursingbusiness.industryReceptors IgGCoculture TechniquesCell biologyRatsStrokeEndocrinologymedicine.anatomical_structureC-Reactive ProteinBlood-Brain BarrierPhosphorylationNeurology (clinical)Endothelium VascularSignal transductionCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesOxidative stressSignal TransductionStroke
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Chronic heart damage following doxorubicin treatment is alleviated by lovastatin.

2014

The anticancer efficacy of anthracyclines is limited by cumulative dose-dependent early and delayed cardiotoxicity resulting in congestive heart failure. Mechanisms responsible for anthracycline-induced heart damage are controversially discussed and effective preventive measures are preferable. Here, we analyzed the influence of the lipid lowering drug lovastatin on anthracycline-induced late cardiotoxicity three month after treatment of C57BL/6 mice with five low doses of doxorubicin (5×3mg/kg BW; i.p.). Doxorubicin increased the cardiac mRNA levels of BNP, IL-6 and CTGF, while the expression of ANP remained unchanged. Lovastatin counteracted these persisting cardiac stress responses evoke…

medicine.medical_specialtyStatinCardiotonic AgentsAnthracyclinemedicine.drug_classBiologymedicine.disease_causeDNA MitochondrialInternal medicineNatriuretic Peptide Brainpolycyclic compoundsmedicineAnimalsDoxorubicinHSP70 Heat-Shock ProteinsLovastatinPharmacologyCardiotoxicityEjection fractionAntibiotics AntineoplasticInterleukin-6Gene Expression ProfilingMyocardiumConnective Tissue Growth Factormedicine.diseaseFibrosisCardiotoxicityMice Inbred C57BLEndocrinologyDoxorubicinHeart failureFemaleLovastatinOxidative stressmedicine.drugDNA DamagePharmacological research
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