Search results for "Cell proliferation"

showing 10 items of 1056 documents

Decreased cell proliferation and higher oxidative stress in fibroblasts from Down Syndrome fetuses. Preliminary study

2013

Abstract Down Syndrome is the most common chromosomal disease and is also known for its decreased incidence of solid tumors and its progeroid phenotype. Cellular and systemic oxidative stress has been considered as one of the Down Syndrome phenotype causes. We correlated, in a preliminary study, the fibroblast proliferation rate and different cell proliferation key regulators, like Rcan1 and the telomere length from Down Syndrome fetuses, with their oxidative stress profile and the Ribonucleic acid and protein expression of the main antioxidant enzymes together with their activity. Increased oxidized glutathione/glutathione ratio and high peroxide production were found in our cell model. Th…

Malemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentPrimary Cell CultureSuperoxide dismutasemedicine.disease_causeSuperoxide dismutasechemistry.chemical_compoundFetusSuperoxide Dismutase-1ThioredoxinsInternal medicineGlutaredoxinmedicineHumansThioredoxinMolecular BiologyGlutaredoxinsCell ProliferationSkinchemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseTelomere lengthbiologyGlutathione peroxidaseTelomere HomeostasisGlutathioneRcan1FibroblastsTelomereCatalaseGlutathioneProgeroidOxidative StressEndocrinologychemistryBiochemistryGene Expression Regulationbiology.proteinMolecular MedicineFemaleThioredoxinDown SyndromeOxidative stressSignal TransductionBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Liver-specific p38α deficiency causes reduced cell growth and cytokinesis failure during chronic biliary cirrhosis in mice

2012

p38α mitogen-activated protein kinases (MAPK) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor β, tumor necrosis factor-α, interleukin-1β, and oxidative stress. p38 MAPK activation results in hepatocyte growth arrest, whereas increased proliferation has been considered a hallmark of p38α-deficient cells. Our aim was to assess the role of p38α in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis. Cholestasis was induced in wildtype and liver-specific p38α knockout mice by…

Malemedicine.medical_specialtyBiliary cirrhosisMAP Kinase Kinase 2ApoptosisBiologymedicine.disease_causeProinflammatory cytokineMitogen-Activated Protein Kinase 14MiceCholestasisInternal medicinemedicineAnimalsCyclin D1Cyclin B1Cell ProliferationCytokinesisMice KnockoutHepatologyLiver Cirrhosis BiliaryHepatologymedicine.diseaseMice Inbred C57BLSurvival RateDisease Models AnimalOxidative Stressmedicine.anatomical_structureEndocrinologyLiverHepatocyteChronic DiseaseDisease ProgressionHepatocytesTumor necrosis factor alphaOxidative stressSignal TransductionTransforming growth factorHepatology
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The selective cyclooxygenase-1 inhibitor SC-560 suppresses cell proliferation and induces apoptosis in human hepatocellular carcinoma cells

2006

Two isoforms of cyclooxygenase (COX) are known, and to date most studies have implicated COX-2 in the development and progression of various human cancers. Increasing evidence suggests that COX-1 may also play a similar role. Indeed, we have recently observed that the dual COX-1/COX-2 inhibitor indomethacin induces apoptosis in human hepatocellular carcinoma (HCC) cell lines more effectively than the selective COX-2 inhibitors, possibly implicating COX-1 in HCC. In this study we investigated the expression of COX-1 in non-tumor and malignant human liver tissues, as well as the effects of the highly selective COX-1 inhibitor SC-560 on cell growth and apoptosis in human HCC cell lines. Expres…

Malemedicine.medical_specialtyCarcinoma HepatocellularCellApoptosisBiologyGene Expression Regulation EnzymologicCell Line TumorInternal medicineSurvivinGeneticsmedicineHumansCyclooxygenase InhibitorCyclooxygenase InhibitorsRNA MessengerAgedCell ProliferationOncogeneCell growthApoptosiGeneral MedicineMiddle AgedCell cycleImmunohistochemistryXIAPGene Expression Regulation NeoplasticEndocrinologymedicine.anatomical_structureCyclooxygenase 2ApoptosisCell culturePyrazoleCyclooxygenase 1Cancer researchPyrazolesFemaleHumanInternational Journal of Molecular Medicine
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Glucagon-like peptide-2 and mouse intestinal adaptation to a high-fat diet.

2013

Endogenous glucagon-like peptide-2 (GLP2) is a key mediator of refeeding-induced and resection-induced intestinal adaptive growth. This study investigated the potential role of GLP2 in mediating the mucosal responses to a chronic high-fat diet (HFD). In this view, the murine small intestine adaptive response to a HFD was analyzed and a possible involvement of endogenous GLP2 was verified using GLP2 (3–33) as GLP2 receptor (GLP2R) antagonist. In comparison with animals fed a standard diet, mice fed a HFD for 14 weeks exhibited an increase in crypt–villus mean height (duodenum, 27.5±3.0%; jejunum, 36.5±2.9%;P<0.01), in the cell number per villus (duodenum, 28.4±2.2%; jejunum, 32.0±2.9%;P&l…

Malemedicine.medical_specialtyDuodenumEndocrinology Diabetes and MetabolismEndogenyBiologyDiet High-Fatdigestive systemJejunumMiceEndocrinologyInternal medicineIntestine SmallmedicineGlucagon-Like Peptide 2Receptors GlucagonAnimalsMolecular Targeted TherapyObesityIntestinal MucosaReceptorCell ProliferationCell growthdigestive oral and skin physiologyGLP2 receptor expression intestinal morphometry obesity intestinal adaptationGlucagon-like peptide-2Adaptation PhysiologicalSmall intestinePeptide FragmentsUp-RegulationMice Inbred C57BLEndocrinologymedicine.anatomical_structureJejunumKi-67 AntigenDuodenumGlucagon-Like Peptide-2 ReceptorAnti-Obesity AgentsGlucagon-Like Peptide-2 ReceptorSignal TransductionThe Journal of endocrinology
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MORT1/FADD is involved in liver regeneration

2006

AIM: To explore the role of the adaptor molecule in liver regeneration after partial hepatectomy (PH). METHODS: We used transgenic mice expressing an N-terminal truncated form of MORT1/FADD under the control of the albumin promoter. As previously shown, this transgenic protein abrogated CD95- and CD120a-mediated apoptosis in the liver. Cyclin A expression was detected using Western blotting. ELISA and RT-PCR were used to detect IL-6 and IL-6 mRNA, respectively. DNA synthesis in liver tissue was measured by BrdU staining. RESULTS: Resection of 70% of the liver was followed by a reduced early regenerative response in the transgenic group at 36 h. Accordingly, 36 h after hepatectomy, cyclin A …

Malemedicine.medical_specialtyFas-Associated Death Domain Proteinmedicine.medical_treatmentTransgeneCyclin AApoptosisMice TransgenicCyclin AMiceInternal medicinemedicineAnimalsHepatectomyFADDAdaptor Proteins Signal TransducingCell ProliferationbiologyInterleukin-6GastroenterologyGeneral MedicineFas receptorMolecular biologyPeptide FragmentsLiver regenerationLiver RegenerationBlotBasic ResearchEndocrinologyApoptosisbiology.proteinHepatectomyWorld Journal of Gastroenterology
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Paradoxically, iron overload does not potentiate doxorubicin-induced cardiotoxicity in vitro in cardiomyocytes and in vivo in mice

2015

Doxorubicin (DOX) is known to induce serious cardiotoxicity, which is believed to be mediated by oxidative stress and complex interactions with iron. However, the relationship between iron and DOX-induced cardiotoxicity remains controversial and the role of iron chelation therapy to prevent cardiotoxicity is called into question. Firstly, we evaluated in vitro the effects of DOX in combination with dextran-iron on cell viability in cultured H9c2 cardiomyocytes and EMT-6 cancer cells. Secondly, we used an in vivo murine model of iron overloading (IO) in which male C57BL/6 mice received a daily intra-peritoneal injection of dextran-iron (15mg/kg) for 3weeks (D0-D20) and then (D21) a single su…

Malemedicine.medical_specialtyIron OverloadCell SurvivalHeart VentriclesIronCardiomegaly030204 cardiovascular system & hematologyToxicologymedicine.disease_causeCell LineVentricular MyosinsMice03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemAtrial natriuretic peptideIn vivoCell Line TumorInternal medicineNatriuretic Peptide Brainpolycyclic compoundsmedicineAnimalsMyocytes CardiacDoxorubicinViability assay030304 developmental biologyPharmacology0303 health sciencesCardiotoxicityCell growthChemistryDextransBrain natriuretic peptideCardiotoxicity[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemUp-Regulation3. Good healthMice Inbred C57BLOxidative Stresscell proliferationEndocrinologyDoxorubicincardiovascular systemOxidative stressmedicine.drugToxicology and Applied Pharmacology
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Benfotiamine accelerates the healing of ischaemic diabetic limbs in mice through protein kinase B/Akt-mediated potentiation of angiogenesis and inhib…

2006

Benfotiamine, a vitamin B1 analogue, reportedly prevents diabetic microangiopathy. The aim of this study was to evaluate whether benfotiamine is of benefit in reparative neovascularisation using a type I diabetes model of hindlimb ischaemia. We also investigated the involvement of protein kinase B (PKB)/Akt in the therapeutic effects of benfotiamine. Streptozotocin-induced diabetic mice, given oral benfotiamine or vehicle, were subjected to unilateral limb ischaemia. Reparative neovascularisation was analysed by histology. The expression of Nos3 and Casp3 was evaluated by real-time PCR, and the activation state of PKB/Akt was assessed by western blot analysis and immunohistochemistry. The f…

Malemedicine.medical_specialtyProgrammed cell deathAngiogenesisEndocrinology Diabetes and MetabolismBlotting WesternNeovascularization PhysiologicApoptosisMice Inbred StrainsBiologyDiabetes Mellitus ExperimentalNeovascularizationMiceRandom AllocationIschemiaInternal medicineInternal MedicinemedicineAnimalsThiamineMuscle SkeletalProtein kinase BCell ProliferationCaspase 3Stem Cellsprotein kinase PKB/AktBody WeightHemodynamicsEndothelial CellsCaspase InhibitorsImmunohistochemistryEndothelial stem cellEnzyme ActivationOxidative StressEndocrinologyBenfotiamineApoptosisCaspasesDietary SupplementsTransketolase activitymedicine.symptomProto-Oncogene Proteins c-aktDiabetic Angiopathiesmedicine.drugDiabetologia
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Characterization of a T-cell-derived mast cell costimulatory activity (MCA) that acts synergistically with interleukin 3 and interleukin 4 on the gro…

1990

The proliferation of mucosal mast cells (MMC) depends on the presence of interleukin 3 (IL 3) and can be further enhanced by interleukin 4 (IL 4). The supernatant of a TH2 cell clone (ST2/K.9) stimulated by concanavalin A was found to contain a factor, provisionally termed mast cell costimulatory activity (MCA), that substantially enhances the proliferation of MMC promoted by a combination of IL 3 and IL 4. In comparison to other lymphokines MCA is rather resistant to tryptic digestion but is very sensitive to pH values lower than 6.0 and to organic solvents. Chromatographic fractionation of MCA revealed that activity is associated with protein(s) or glycoprotein(s) of 35 to 40 kDa. Partial…

Malemedicine.medical_specialtyT-LymphocytesImmunologyBone Marrow CellsBiologyBiochemistryMast cell proliferationCell LineBiological FactorsMiceEpidermal growth factorInternal medicinemedicineImmunology and AllergyAnimalsMast CellsMolecular BiologyInterleukin 4Interleukin 3LymphokinesLymphokineDrug SynergismHematologyMast cellHematopoietic Stem CellsMolecular biologyClone Cellsmedicine.anatomical_structureEndocrinologyMice Inbred DBAChromatography GelCytokinesTumor necrosis factor alphaFemaleInterleukin-3Interleukin-4Leukemia inhibitory factorCell DivisionCytokine
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Optical Coherence Tomography Versus Intravascular Ultrasound to Evaluate Coronary Artery Disease and Percutaneous Coronary Intervention

2013

ObjectivesWe compared intravascular ultrasound (IVUS) and 2 different generations of optical coherence tomography (OCT)—time-domain OCT (TD-OCT) and frequency-domain OCT (FD-OCT)—for the assessment of coronary disease and percutaneous coronary intervention (PCI) using stents.BackgroundOCT is a promising light-based intravascular imaging modality with higher resolution than IVUS. However, the paucity of data on OCT image quantification has limited its application in clinical practice.MethodsA total of 227 matched OCT and IVUS pull backs were studied. One hundred FD-OCT and IVUS pull backs in nonstented (n = 56) and stented (n = 44) vessels were compared. Additionally, 127 matched TD-OCT and …

Malemedicine.medical_specialtyTime Factorsgenetic structuresmedicine.medical_treatmentTreatment outcomeSeverity of Illness Indexintravascular ultrasoundCoronary RestenosisCoronary artery diseaseOptical coherence tomographyPredictive Value of TestsNeointimaIntravascular ultrasoundmedicineHumanscardiovascular diseasesUltrasonography InterventionalAgedCell ProliferationAnalysis of VarianceHyperplasiaoptical coherence tomographymedicine.diagnostic_testbusiness.industrypercutaneous coronary interventionCoronary StenosisPercutaneous coronary interventionMiddle Agedequipment and suppliesmedicine.diseaseCoronary Vesselseye diseasesTreatment Outcomesurgical procedures operativeLinear ModelsFemaleStentssense organsTomographyRadiologyUltrasonographybusinessCardiology and Cardiovascular MedicineTomography Optical CoherenceJACC: Cardiovascular Interventions
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The Fate of Nephrons in Congenital Obstructive Nephropathy: Adult Recovery is Limited by Nephron Number Despite Early Release of Obstruction

2015

Urinary tract obstruction and reduced nephron number often occur together as a result of maldevelopment of the kidneys and the urinary tract. We determined the role of nephron number on adaptation of the remaining nephrons of mice subjected to neonatal partial unilateral ureteral obstruction followed through adulthood.Wild-type and Os/+ mice (the latter with 50% fewer nephrons) underwent sham operation or partial unilateral ureteral obstruction in the first 2 days of life. Additional mice underwent release of unilateral ureteral obstruction at 7 days. All kidneys were harvested at 3 weeks (weaning) or 6 weeks (adulthood). Glomerular number and area, glomerulotubular junction integrity, prox…

Malemedicine.medical_specialtyUrologyUrinary systemKidney GlomerulusUrologygrowth and developmentCell CountNephronurologic and male genital diseasesArticleureteral obstructionMiceMaldevelopmentInternal medicinemedicineAnimalsWeaningdisease progression; growth and development; nephrons; ureteral obstructionRenal InsufficiencyCell ProliferationKidneyDisease progressionurogenital systembusiness.industrySettore MED/20 - Chirurgia Pediatrica E InfantileNephronsKidney Glomerulusmedicine.diseasenephronObstructive NephropathyDisease Models Animalmedicine.anatomical_structureEndocrinologyAnimals NewbornFemaleUrinary tract obstructionbusiness
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