Search results for "PROLIFERATION"

showing 10 items of 1193 documents

Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

2011

Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described …

MaleMAPK/ERK pathwayAgingMAP Kinase Signaling SystemCancer aging RAF MEK mTORApoptosisReviewBiologyPI3KModels BiologicalApoptosis; Cancer; Kinases; MEK; MTOR; PI3K; Protein phosphorylation; RAF; Signal transductionMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCancer stem cellNeoplasmscancerAnimalsHumansPTENProtein kinase BCellular SenescencePI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesKinaseTOR Serine-Threonine KinasesapoptosisPTEN PhosphohydrolaseRafCell BiologyMEKprotein phosphorylation3. Good healthCell biologyCrosstalk (biology)kinases030220 oncology & carcinogenesisMutationmTORCancer researchbiology.proteinFemaleraf KinasesProto-Oncogene Proteins c-aktCell agingsignal transduction
researchProduct

Plasticity-related gene-1 inhibits lysophosphatidic acid-induced vascular smooth muscle cell migration and proliferation and prevents neointima forma…

2012

International audience; Plasticity-related gene-1 (PRG-1) protects neuronal cells from lysophosphatidic acid (LPA) effects. In vascular smooth muscle cells (VSMCs), LPA was shown to induce phenotypic modulation in vitro and vascular remodeling in vivo. Thus we explored the role of PRG-1 in modulating VSMC response to LPA. PCR, Western blot, and immunofluorescence experiments showed that PRG-1 is expressed in rat and human vascular media. PRG-1 expression was strongly inhibited in proliferating compared with quiescent VSMCs both in vitro and in vivo (medial vs. neointimal VSMCs), suggesting that PRG-1 expression is dependent on the cell phenotype. In vitro, adenovirus-mediated overexpression…

MaleMAPK/ERK pathwayNeointimaVascular smooth musclePhysiologyPhenotypic modulation[SDV]Life Sciences [q-bio]Genetic VectorsBiologyPlasticityMuscle Smooth VascularAdenoviridaechemistry.chemical_compoundCell MovementNeointimaLysophosphatidic acidAnimalsHumansRats WistarCells CulturedCell ProliferationCell BiologyLipid-phosphate phosphatasePhosphoric Monoester HydrolasesIn vitroRatsCell biologyGene Expression RegulationchemistryBiochemistryCalmodulin-Binding ProteinsLysophospholipidsAmerican Journal of Physiology-Cell Physiology
researchProduct

A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
researchProduct

MUC16 Is Overexpressed in Idiopathic Pulmonary Fibrosis and Induces Fibrotic Responses Mediated by Transforming Growth Factor-β1 Canonical Pathway

2021

Several transmembrane mucins have demonstrated that they contribute intracellularly to induce fibrotic processes. The extracellular domain of MUC16 is considered as a biomarker for disease progression and death in IPF patients. However, there is no evidence regarding the signalling capabilities of MUC16 that contribute to IPF development. Here, we demonstrate that MUC16 was overexpressed in the lung tissue of IPF patients (n = 20) compared with healthy subjects (n = 17) and localised in fibroblasts and hyperplastic alveolar type II cells. Repression of MUC16 expression by siRNA-MUC16 transfection inhibited the TGF-β1-induced fibrotic processes such as mesenchymal/ myofibroblast transformati…

MaleMUC16Gene ExpressionIdiopathic pulmonary fibrosis0302 clinical medicineBiology (General)PhosphorylationMyofibroblastsLungSpectroscopytransforming growth factor betabiologyChemistryGeneral MedicineTransfectionMiddle Agedrespiratory systemidiopathic pulmonary fibrosisImmunohistochemistryRespiratory Function TestsComputer Science ApplicationsChemistrymedicine.anatomical_structure030220 oncology & carcinogenesisFemaleDisease SusceptibilityMyofibroblastSignal TransductionQH301-705.5Models BiologicalArticleCatalysisCell LineTransforming Growth Factor beta1Inorganic Chemistry03 medical and health sciencesmedicineHumansPhysical and Theoretical ChemistryFibroblastQD1-999Molecular BiologyAgedCell ProliferationA549 cellOrganic ChemistryMesenchymal stem cellMembrane ProteinsTransforming growth factor betaFibroblastsmedicine.diseaserespiratory tract diseases030228 respiratory systemCA-125 AntigenCase-Control StudiesCancer researchbiology.proteinIdiopathic Pulmonary Fibrosis ; Muc16 ; Transforming Growth Factor BetaBiomarkersTransforming growth factorInternational Journal of Molecular Sciences
researchProduct

Circulating CSF-1 Promotes Monocyte and Macrophage Phenotypes that Enhance Lupus Nephritis

2009

Macrophages mediate kidney disease and are prominent in a mouse model (MRL- Fas lpr ) of lupus nephritis. Colony stimulating factor-1 (CSF-1) is the primary growth factor for macrophages, and CSF-1 deficiency protects MRL- Fas lpr mice from kidney disease and systemic illness. Whether this renoprotection derives from a reduction of macrophages and whether systemic CSF-1, as opposed to intrarenal CSF-1, promotes macrophage-dependent lupus nephritis remain unclear. Here, we found that increasing systemic CSF-1 hastened the onset of lupus nephritis in MRL- Fas lpr mice. Using mutant MRL- Fas lpr strains that express high, moderate, or no systemic CSF-1, we detected a much higher tempo of kidne…

MaleMacrophage colony-stimulating factorMice Inbred MRL lprLupus nephritisMice TransgenicInflammationKidneyMonocytesMiceimmune system diseasesmedicineAnimalsHumansskin and connective tissue diseasesCell ProliferationInflammationMice Inbred BALB CMice Inbred C3HSystemic lupus erythematosusbiologyCD68business.industryMacrophage Colony-Stimulating FactorMacrophagesMonocyteGeneral MedicineMonocyte proliferationmedicine.diseaseLupus NephritisMice Inbred C57BLDisease Models AnimalBasic ResearchPhenotypemedicine.anatomical_structureIntegrin alpha MNephrologyImmunologybiology.proteinFemalemedicine.symptombusinessJournal of the American Society of Nephrology
researchProduct

Sevoflurane affects neurogenesis after forebrain ischemia in rats.

2007

BACKGROUND: The effect of sevoflurane on the neuroregenerative potential after neuronal injury is unclear. We investigated the effect of low and high concentrations of sevoflurane on endogenous neurogenesis after cerebral ischemia. METHODS: Anesthetized and ventilated rats were randomized to four different treatment groups. Groups 1 and 2: 1.4% sevoflurane; Groups 3 and 4: 2.8% sevoflurane. In Groups 1 and 3, no cerebral ischemia was induced (sham-operated). In Groups 2 and 4, 10 min of forebrain ischemia was induced by bilateral carotid artery occlusion plus hemorrhagic hypotension. Physiological variables were maintained constant. Bromodeoxyuridine was given as a marker of neurogenesis. A…

MaleMethyl EthersIschemiaH&E stainHippocampusHippocampusSevofluraneBrain IschemiaRats Sprague-Dawleychemistry.chemical_compoundRandom AllocationSevofluraneProsencephalonmedicineAnimalsCell ProliferationNeuronsDose-Response Relationship Drugbusiness.industryDentate gyrusNeurogenesismedicine.diseaseNerve RegenerationRatsDose–response relationshipDisease Models AnimalAnesthesiology and Pain MedicinechemistryAnesthesiaAnesthetics InhalationDentate GyrusbusinessBromodeoxyuridinemedicine.drugAnesthesia and analgesia
researchProduct

Mild Hypothermia Has No Long-Term Impact on Postischemic Neurogenesis in Rats

2009

Postischemic improvement of functional outcome by therapeutic hypothermia may be related to cerebral regeneration by postischemic neurogenesis. We investigated whether mild peri-ischemic hypothermia leads to a long-term increase in postischemic neurogenesis.Seventy male sevoflurane-anesthetized Sprague Dawley rats were randomly assigned to the following treatment groups: normothermic ischemia, intraischemic hypothermia, and postischemic hypothermia with corresponding sham-operated controls. Fifteen naïve rats were investigated as reference for natural neurogenesis. Forebrain ischemia was induced by bilateral common carotid artery occlusion and hemorrhagic hypotension. In normothermic groups…

MaleMild hypothermiaTime FactorsNeurogenesisIschemiaSeverity of Illness IndexBrain IschemiaRats Sprague-DawleyProsencephalonHypothermia InducedmedicineAnimalsCell ProliferationNeuronsbusiness.industryNeurogenesisHypothermiamedicine.diseaseRatsSprague dawleyDisease Models AnimalAnesthesiology and Pain MedicineAnesthesiaDentate GyrusNerve Degenerationmedicine.symptombusinessAnesthesia & Analgesia
researchProduct

Intramural delivery of Sirolimus prevents vascular remodeling following balloon injury

2005

Abstract Objective. Several studies have demonstrated that Sirolimus-eluting stents reduce restenosis in patients with coronary artery disease. Here, we tested whether direct delivery of Sirolimus into the vessel wall during balloon angioplasty can modify vascular remodeling over several weeks. Methods and Results. During angioplasty of the rabbit iliac artery we administered an intramural infusion of Sirolimus or its vehicle directly through a balloon catheter into the vessel wall. After 3 weeks neointimal formation was decreased (0.71 ± 0.1 vs. 1.4 ± 0.12 intima/media ratio), and this process was attributed to the inhibitory properties of Sirolimus on ECM deposition and smooth muscle cell…

MaleNeointimaPathologymedicine.medical_specialtymedicine.medical_treatmentBiophysicsBalloonIliac ArteryBiochemistryMuscle Smooth VascularArticleAnalytical ChemistryRestenosisAngioplastymedicineAnimalsVimentincardiovascular diseasesMolecular BiologyCell ProliferationSirolimusbiologybusiness.industryGraft Occlusion VascularBalloon catheterequipment and suppliesmedicine.diseaseTunica intimaActinsExtracellular MatrixFibronectinsCollagen Type IIImedicine.anatomical_structurealpha 1-AntitrypsinSirolimuscardiovascular systembiology.proteinLamininRabbitsTunica IntimabusinessElastinAngioplasty Balloonmedicine.drugBiochimica et Biophysica Acta (BBA) - Proteins and Proteomics
researchProduct

Quiescence Modulates Stem Cell Maintenance and Regenerative Capacity in the Aging Brain.

2018

The function of somatic stem cells declines with age. Understanding the molecular underpinnings of this decline is key to counteract age-related disease. Here, we report a dramatic drop in the neural stem cells (NSCs) number in the aging murine brain. We find that this smaller stem cell reservoir is protected from full depletion by an increase in quiescence that makes old NSCs more resistant to regenerate the injured brain. Once activated, however, young and old NSCs show similar proliferation and differentiation capacity. Single-cell transcriptomics of NSCs indicate that aging changes NSCs minimally. In the aging brain, niche-derived inflammatory signals and the Wnt antagonist sFRP5 induce…

MaleNeurogenesisSubventricular zoneInflammationBiologyGeneral Biochemistry Genetics and Molecular BiologyTranscriptome03 medical and health sciencesMice0302 clinical medicineNeural Stem CellsmedicineAging brainsFRP5stem cell agingAnimalsHomeostasisquiescenceStem Cell Nichereproductive and urinary physiologyCellular Senescence030304 developmental biologyneural stem cellsCell Proliferation0303 health sciencesWnt signaling pathwayAge Factorssubventricular zoneBrainmodelingCell DifferentiationinterferonWnt signalingNeural stem cellCell biologynervous system diseasesNerve RegenerationMice Inbred C57BLmedicine.anatomical_structurenervous systeminflammationsimulationsmedicine.symptomStem cellbiological phenomena cell phenomena and immunitysingle-cell transcriptomics030217 neurology & neurosurgeryCell DivisionAdult stem cellCell
researchProduct

Acute intermittent nicotine treatment induces fibroblast growth factor-2 in the subventricular zone of the adult rat brain and enhances neuronal prec…

2007

Abstract Over the past years, evidence has accumulated that stem cells are present in the adult brain, and generate neurons and/or glia from two active germinal zones: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus. This study shows that acute intermittent nicotine treatment significantly enhances neuronal precursor cell proliferation in the SVZ of adult rat brain, but not in the SGZ of the hippocampus, and pre-treatment with mecamylamine, a nonselective nAChR antagonist, blocks the enhanced precursor proliferation by nicotine. This effect is supported by up-regulation of fibroblast growth factor-2 (FGF-2) mRNA …

MaleNicotinemedicine.medical_specialtyBasic fibroblast growth factorSubventricular zoneNicotinic AntagonistsReceptors NicotinicBiologyFibroblast growth factorSettore BIO/09 - FisiologiaHippocampusSubgranular zonechemistry.chemical_compoundLateral VentriclesInternal medicinePrecursor cellmedicineAnimalsPyrrolesNicotinic AgonistsRNA MessengerReceptor Fibroblast Growth Factor Type 1Rats WistarCell ProliferationNeuronsNeuronal PlasticityStem CellsGeneral NeuroscienceFibroblast growth factor receptor 1Dentate gyrusNeurogenesisCell DifferentiationNerve RegenerationRatsUp-RegulationCell biologymedicine.anatomical_structureEndocrinologynervous systemchemistryneurogenesis FGF-2 FGFR-1 subventricular zone nicotineFibroblast Growth Factor 2Neuroscience
researchProduct