Search results for " growth factor"

showing 10 items of 1227 documents

The alpha and ßeta in phase II trials hepatocellular carcinoma ‐ A tale of more than radiological response?

2019

Carcinoma HepatocellularHepatologybusiness.industryLiver NeoplasmsReceptor Transforming Growth Factor-beta Type IAlpha (ethology)Setamedicine.diseaseRadiological weaponHepatocellular carcinomaQuinolinesHumansPyrazolesMedicinebusinessNuclear medicineLiver International
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Expression of WISPs and of their novel alternative variants in human hepatocellular carcinoma cells

2005

WISPs (Wnt-induced secreted proteins) are members of the CCN (CTGF/Cyr61/Nov) family involved in fibrotic disorders and tumorigenesis. They have a typical structure composed of four conserved cysteine-rich modular domains, but variants of CCN members lacking one or more modules, generated by alternative splicing or gene mutations, have been described in various pathological conditions. WISP genes were first described as downstream targets of the Wnt signaling pathway, which is frequently altered in human hepatocellular carcinoma (HCC). In the present study, WISP mRNA expression was analyzed by RT-PCR in four human HCC cell lines (HepG2, HuH-6, HuH-7, HA22T/VGH). Our results show for the fir…

Carcinoma HepatocellularWISPHepatocellular carcinomaApoptosisGene mutationBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCCN Intercellular Signaling ProteinsWntalternative splicingHistory and Philosophy of ScienceCell Line TumorProto-Oncogene ProteinsCCN Intercellular Signaling ProteinsmedicineHumansRNA MessengerGeneDNA PrimersOncogene ProteinsGeneticsCCNModels GeneticReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceLiver NeoplasmsAlternative splicingIntracellular Signaling Peptides and ProteinsWnt signaling pathwaydigestive system diseasesNeoplasm ProteinsInsulin-Like Growth Factor Binding ProteinsRepressor ProteinsCTGFCYR61Cancer researchIntercellular Signaling Peptides and ProteinsRNACarcinogenesisWISPWntTranscription Factors
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2021

Growth and differentiation factor 15 (GDF15) belongs to the transforming growth factor-β (TGF-β) superfamily of proteins. Glial-derived neurotrophic factor (GDNF) family receptor α-like (GFRAL) is an endogenous receptor for GDF15 detected selectively in the brain. GDF15 is not normally expressed in the tissue but is prominently induced by “injury”. Serum levels of GDF15 are also increased by aging and in response to cellular stress and mitochondrial dysfunction. It acts as an inflammatory marker and plays a role in the pathogenesis of cardiovascular diseases, metabolic disorders, and neurodegenerative processes. Identified as a new heart-derived endocrine hormone that regulates body growth,…

Cardiac fibrosis030204 cardiovascular system & hematologyCatalysisInorganic Chemistry03 medical and health sciencesParacrine signalling0302 clinical medicineNeurotrophic factorsGlial cell line-derived neurotrophic factorMedicinePhysical and Theoretical ChemistryReceptorAutocrine signallingMolecular BiologySpectroscopy030304 developmental biology0303 health sciencesbiologybusiness.industryOrganic ChemistryGeneral Medicinemedicine.disease3. Good healthComputer Science Applicationsbiology.proteinCancer researchGDF15businessTransforming growth factorInternational Journal of Molecular Sciences
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Cardioprotection by gene therapy

2015

Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…

Cardioprotectionmedicine.medical_specialtybiologybusiness.industryGene targetingSphingosine kinase 1Heat shock proteinInternal medicineGene expressionmedicinebiology.proteinCardiologyHepatocyte growth factorSignal transductionCardiology and Cardiovascular MedicinebusinessTranscription factormedicine.drugInternational Journal of Cardiology
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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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Haem oxygenase-1 regulates catabolic and anabolic processes in osteoarthritic chondrocytes

2007

Pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and other catabolic factors participate in the pathogenesis of cartilage damage in osteoarthritis (OA). Pro-inflammatory cytokines such as interleukin-1β (IL-1β) mediate cartilage degradation and might be involved in the progression of OA. Previously, we found that haem oxygenase-1 (HO-1) is down-regulated by pro-inflammatory cytokines and up-regulated by IL-10 in OA chondrocytes. The aim of this study was to determine whether HO-1 can modify the catabolic effects of IL-1β in OA cartilage and chondrocytes. Up-regulation of HO-1 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL-1β in OA …

Cartilage ArticularMaleMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaProtoporphyrinsMatrix metalloproteinaseChondrocytePathology and Forensic MedicineExtracellular matrixChondrocytesmedicineExtracellularHumansInsulin-Like Growth Factor ICollagen Type IICells CulturedAggrecanAgedbiologyChemistryCartilageGrowth factorOsteoarthritis KneeMatrix MetalloproteinasesCell biologymedicine.anatomical_structureProteoglycanImmunologybiology.proteinFemaleProteoglycansHeme Oxygenase-1The Journal of Pathology
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Insulin-like growth factors counteract the effect of interleukin 1 beta on type II phospholipase A2 expression and arachidonic acid release by rabbit…

1994

International audience; Interleukin 1 beta was found to stimulate arachidonic acid release, and the synthesis and secretion of type II phospholipase A2 by rabbit articular chondrocytes in vitro. Interleukin 1 beta had no effect on the level of cytosolic phospholipase A2 mRNA. Insulin-like growth factors, which help stabilize the cartilage matrix, reduced the effect of interleukin 1 beta on type II phospholipase A2 activity and mRNA level, and decreased the Interleukin 1 beta-stimulated arachidonic acid release to the basal values. This suggests that type II phospholipase A2 plays a key role in arachidonic acid release from rabbit articular chondrocytes and that insulin-like growth factors c…

Cartilage Articularmedicine.medical_specialtymedicine.medical_treatmentBiophysicsIn Vitro TechniquesBiochemistryChondrocytePhospholipases AInterleukin 1βInsulin-like growth factorchemistry.chemical_compoundPhospholipase A2[ CHIM.ORGA ] Chemical Sciences/Organic chemistryPhospholipase A2Structural BiologyInsulin-Like Growth Factor IIInternal medicineGeneticsmedicineAnimalsInsulin-like growth factorRNA MessengerInsulin-Like Growth Factor IMolecular BiologyArachidonic Acidbiology[CHIM.ORGA]Chemical Sciences/Organic chemistryArthritisInterleukinCell Biology[CHIM.ORGA] Chemical Sciences/Organic chemistryChondrocyteSomatomedinPhospholipases A2Endocrinologymedicine.anatomical_structureCytokinechemistryInsulin-like growth factor 2biology.proteinArachidonic acidRabbitsInterleukin-1
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Kinetic and thermodynamic insights into interaction of erlotinib with epidermal growth factor receptor: Surface plasmon resonance and molecular docki…

2020

Abstract Epidermal growth factor receptor (EGFR) plays an important role in cell proliferation at non-small cell lung cancer (NSCLC). Therefore, targeted therapy of cancer via this kind of receptor is highly interested. Small molecule drugs such as erlotinib and gefitinib inhibit EGFR tyrosine kinase and thus suppress cell proliferation. At this paper, erlotinib interaction with EGFR on the cell surface was studied via surface plasmon resonance (SPR) and molecular docking methods. Kinetic parameters indicated that erlotinib affinity toward EGFR was increased through increment of temperature. The thermodynamic analysis showed that van der Waals and hydrogen binding forces play a major role i…

Cell Culture TechniquesQuantitative Structure-Activity RelationshipAntineoplastic Agents02 engineering and technologyMolecular Dynamics SimulationBiochemistry03 medical and health sciencesErlotinib HydrochlorideGefitinibStructural BiologymedicineHumansheterocyclic compoundsEpidermal growth factor receptorSurface plasmon resonanceReceptorneoplasmsMolecular BiologyProtein Kinase Inhibitors030304 developmental biology0303 health sciencesBinding SitesbiologyChemistryCell growthGeneral MedicineSurface Plasmon Resonance021001 nanoscience & nanotechnologySmall moleculerespiratory tract diseasesErbB ReceptorsMolecular Docking SimulationKineticsDocking (molecular)biology.proteinBiophysicsThermodynamicsErlotinib0210 nano-technologymedicine.drugProtein BindingInternational journal of biological macromolecules
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Kinetic models for nucleocytoplasmic transport of messenger RNA

1995

Abstract Much is known about the mechanism by which mRNAs cross the nuclear envelope (the translocation stage of nucleocytoplasmic transport), but far less is known about the preceding (intranuclear migration/release) and succeeding (cytoplasmic binding) stages. Therefore, existing information suffices for articulating detailed kinetic models of translocation, but not models for the overall mRNA transport process. In this paper, we show that simple kinetic models of translocation can (i) accommodate date about nucleocytoplasmic distributions of endogenous transcripts; (ii) predict the overall effects on these distributions of effectors such as insulin and epidermal growth factor; (iii) thro…

Cell NucleusStatistics and ProbabilityCytoplasmMessenger RNAModels GeneticGeneral Immunology and MicrobiologyMechanism (biology)EffectorApplied MathematicsChromosomal translocationGeneral MedicineBiologyTranslocation GeneticGeneral Biochemistry Genetics and Molecular BiologyCell biologyKineticsBiochemistryNucleocytoplasmic TransportEpidermal growth factorCytoplasmModeling and SimulationAnimalsMRNA transportRNA MessengerGeneral Agricultural and Biological SciencesJournal of Theoretical Biology
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Central nicotinic receptors, neurotrophic factors and neuroprotection

2000

The multiple combinations of nAChR subunits identified in central nervous structures possess distinct pharmacological and physiological properties. A growing number of data have shown that compounds interacting with neuronal nAChRs have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improving of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Epidemiological and clinical studies suggested also a potential neuroprotective/trophic role of (-)-nicotine in neurodegenerative disease, such as Alzheimer's and Parkinson's disease. Taken together experimental and clinical data largely ind…

Cell SurvivalAgonist-antagonistCentral nervous systemReceptors Nicotiniccomplex mixturesNeuroprotectionBehavioral NeuroscienceNeurotrophic factorsmental disordersmedicineAnimalsHumansNerve Growth FactorsAcetylcholine receptorNeuronsRegulation of gene expressionbiologymusculoskeletal neural and ocular physiologyBrainHaplorhinimedicine.diseaseRatsNeuroprotective Agentsmedicine.anatomical_structurenervous systembiology.proteinFibroblast Growth Factor 2sense organsAlzheimer's diseasePsychologyNeuroscienceNeurotrophinBehavioural Brain Research
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