Search results for "Fibroblast growth factor"

showing 10 items of 129 documents

Nicotine-induced fibroblast growth factor-2 restores the age-related decline of precursor cell proliferation in the subventricular zone of rat brain.

2007

Precursor cell proliferation is present in the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus of adult rat and persists during aging although at reduced levels. Previous studies have shown that acute intermittent nicotine treatment significantly increases fibroblast growth factor-2 (FGF-2) expression in several brain regions of aged rats. The aim of the present investigation was to test the hypothesis that nicotine-induced expression of FGF-2 may restore the age-related decline of precursor cell proliferation. It was first demonstrated that nicotine treatment increases both mRNA and protein FGF-2 in the SVZ of aged …

Malemedicine.medical_specialtyAgingNicotineBasic fibroblast growth factorSubventricular zoneCell CountNerve Tissue ProteinsBiologyFibroblast growth factorSettore BIO/09 - FisiologiaAntibodiesSubgranular zoneNestinchemistry.chemical_compoundIntermediate Filament ProteinsInternal medicinePrecursor cellLateral VentriclesGlial Fibrillary Acidic ProteinmedicineAnimalsNicotinic AgonistsRats WistarMolecular BiologyCell ProliferationAnalysis of VarianceCell growthGeneral NeuroscienceDentate gyrusFibroblast growth factor receptor 1BrainPrecursor proliferationFGF-2 FGFR1 SVZ Nicotine AgedRatsAdult Stem CellsEndocrinologymedicine.anatomical_structurenervous systemchemistryBromodeoxyuridineGene Expression RegulationFibroblast Growth Factor 2Neurology (clinical)Developmental BiologyBrain research
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β-Adrenoceptors differentially regulate vascular tone and angiogenesis of rat aorta via ERK1/2 and p38

2014

β-Adrenoceptors (β-ARs) modulate ERK1/2 and p38 in different cells, but little is known about the contribution of these signaling pathways to the function of β-ARs in vascular tissue. Immunoblotting analysis of rat aortic rings, primary endothelial (ECs) and smooth muscle cells (SMCs) isolated from aorta showed that β-AR stimulation with isoprenaline activated p38 in aortic rings and in both cultured cell types, whereas it had a dual effect on ERK1/2 phosphorylation, decreasing it in ECs while increasing it in SMCs. These effects were reversed by propranolol, which by itself increased p-ERK1/2 in ECs. Isoprenaline β-AR mediated vasodilation of aortic rings was potentiated by the ERK1/2 inhi…

Malemedicine.medical_specialtyEndotheliumPhysiologyAngiogenesisVasodilator AgentsAdrenergic beta-AntagonistsMyocytes Smooth MuscleNeovascularization PhysiologicAorta ThoracicStimulationVasodilationFibroblast growth factorp38 Mitogen-Activated Protein KinasesMuscle Smooth VascularInternal medicineIsoprenalinemedicine.arteryReceptors Adrenergic betamedicineAnimalsHumansRats WistarMitogen-Activated Protein Kinase 1PharmacologyMatrigelAortaMitogen-Activated Protein Kinase 3business.industryAdrenergic beta-AgonistsPropranololRatsVasodilationHEK293 Cellsmedicine.anatomical_structureEndocrinologycardiovascular systemMolecular MedicineEndothelium Vascularbusinessmedicine.drugVascular Pharmacology
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Administration of keratinocyte growth factor down-regulates the pulmonary capacity of acetylcholine production.

2007

Abstract Keratinocyte growth factor protects the lung against various injurious stimuli. The protective mechanisms, however, are not yet fully understood. The aim of this study is to determine the influence of keratinocyte growth factor on the pulmonary capacity to synthesize acetylcholine, a potent regulator of pulmonary functions which is potentially involved in lung damage. Rats were treated twice (days 1 and 2) intratracheally with keratinocyte growth factor and analyzed at day 4. The mRNA expression of choline acetyltransferase – the acetylcholine synthesizing enzyme – was analyzed by real-time RT-PCR in the lung and in isolated alveolar epithelial type II cells. Choline acetyltransfer…

Malemedicine.medical_specialtyFibroblast Growth Factor 7CellDown-RegulationBiologyBiochemistryCholine O-Acetyltransferasechemistry.chemical_compoundInternal medicinemedicineAnimalsRNA MessengerCation Transport ProteinsLungSurfactant homeostasisLungEpithelial CellsPulmonary SurfactantsCell BiologyCholine acetyltransferaseAcetylcholineRecombinant ProteinsRatsCholine transporterEndocrinologymedicine.anatomical_structurechemistryRats Inbred LewKeratinocyte growth factorKeratinocyteAcetylcholinemedicine.drugThe international journal of biochemistrycell biology
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Acute intermittent nicotine treatment produces a reduction in the total number of FGF-2 immunoreactive astroglial cells in the substantia nigra of th…

2004

To understand the morphological substrate of the nicotine effect on nigral FGF-2 expression, a stereological analysis of FGF-2 immunoreactive neuronal and glial profiles has been performed in the substantia nigra of the rat after acute intermittent nicotine treatment. The major finding of this paper is the demonstration that this type of nicotine treatment produces a significant reduction in the total number of nuclear FGF-2 immunoreactive astroglial profiles in the substantia nigra. A parallel analysis of nigral FGF-1 and FGF-5 immunoreactivities showed no effect of this type of nicotine treatment. The results may be explained by an inhibition of FGF-2 synthesis in a subpopulation of nigra…

Malemedicine.medical_specialtyNicotineCentral nervous systemFGF-2Substantia nigraStereologyFGF-1Cell CountBiologyFibroblast growth factornicotine; FGF-2; stereology; immunoreactivity; substantia nigra; FGF-1; FGF-5FGF-5NicotineRats Sprague-DawleyStereotaxic TechniquesInternal medicinemedicineAnimalsGeneral NeuroscienceAlkaloidImmunohistochemistryRatsSubstantia Nigramedicine.anatomical_structureEndocrinologyNicotinic agonistnervous systemsubstantia nigraAstrocytesStereotaxic techniquestereologyFibroblast Growth Factor 2immunoreactivitymedicine.drugnicotineNeuroscience letters
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Evidence for the existence of FGFR1-5-HT1A heteroreceptor complexes in the midbrain raphe 5-HT system.

2015

The ascending midbrain 5-HT neurons known to contain 5-HT1A autoreceptors may be dysregulated in depression due to a reduced trophic support. With in situ proximity ligation assay (PLA) and supported by co-location of the FGFR1 and 5-HT1A immunoreactivities in midbrain raphe 5-HT cells, evidence for the existence of FGFR1–5-HT1A heteroreceptor complexes were obtained in the dorsal and median raphe nuclei of the Sprague–Dawley rat. Their existence in the rat medullary raphe RN33B cell cultures was also established. After combined FGF-2 and 8-OH-DPAT treatment, a marked and significant increase in PLA positive clusters was found in the RN33B cells. Similar results were reached upon coactivati…

Malemedicine.medical_specialtySerotoninG-protein-coupled receptorReceptor tyrosine kinaseBiophysicsHeteroreceptor complexProximity ligation assayBiologyHeteroreceptorBiochemistryMidbrainRats Sprague-DawleyG-protein-coupled receptors; Receptor tyrosine kinases; Fibroblast growth factor receptor 1; Serotonin receptors; Heteroreceptor complex; DimerizationInternal medicinemedicineFluorescence Resonance Energy TransferAnimalsHumansReceptor Fibroblast Growth Factor Type 1Serotonin receptorMolecular Biology5-HT receptorNeurons8-Hydroxy-2-(di-n-propylamino)tetralinRapheMidbrain Raphe NucleiCell BiologyFibroblast growth factor receptor 1Cell biologyRatsmedicine.anatomical_structureEndocrinologyHEK293 Cellsnervous systemGene Expression RegulationReceptor Serotonin 5-HT1AAutoreceptorFibroblast Growth Factor 2NeuronRaphe nucleiPeptidesDimerizationProtein BindingBiochemical and biophysical research communications
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Enzymatically Degraded, Nonoxidized LDL Induces Human Vascular Smooth Muscle Cell Activation, Foam Cell Transformation, and Proliferation

2000

Background —Enzymatic, nonoxidative modification transforms LDL to an atherogenic molecule (E-LDL) that activates complement and macrophages and is present in early atherosclerotic lesions. Methods and Results —We report on the atherogenic effects of E-LDL on human vascular smooth muscle cells (SMC). E-LDL accumulated in these cells, and this was accompanied by selective induction of monocyte chemotactic protein-1 in the absence of effects on the expression of interleukin (IL)-8, RANTES, or monocyte inflammatory proteins-1α and -β). Furthermore, E-LDL stimulated the expression of gp130, the signal-transducing chain of the IL-6 receptor (IL-6R) family, and the secretion of IL-6. E-LDL invok…

Malemedicine.medical_specialtyVascular smooth muscleArteriosclerosismedicine.medical_treatmentBiologyFibroblast growth factorMuscle Smooth VascularStatistics NonparametricPhysiology (medical)Internal medicinemedicineHomeostasisHumansRNA MessengerAutocrine signallingAortaCells CulturedChemokine CCL2AgedFoam cellInterleukin-6Cell growthGrowth factorMonocyteCholesterol LDLReceptors Interleukin-6EnzymesCell biologymedicine.anatomical_structureEndocrinologyFemaleCardiology and Cardiovascular MedicineCell activationOxidation-ReductionCell DivisionFoam CellsCirculation
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UNC-52/perlecan affects gonadal leader cell migrations in C. elegans hermaphrodites through alterations in growth factor signaling.

2003

0012-1606 doi: DOI: 10.1016/S0012-1606(03)00014-9; The unc-52 gene of Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the UNC-6/netrin guidance system. These unc-52 alleles do not cause circumferential DTC migration defects in an otherwise wild-type genetic background. The effects of unc-52 mutations on DTC migrations are distinct from effects on myofilament organization and can be partially suppressed by mutations in several genes encoding growth factor-like molecu…

Malemedicine.medical_treatmentOrganogenesisCellDisorders of Sex DevelopmentReceptor-Like Protein Tyrosine PhosphatasesFibroblast growth factorAnimals Genetically ModifiedCell MovementNetrinGrowth SubstancesGenes HelminthGeneticsMusclesCell migrationsWnt signaling pathwayHelminth Proteinsmedicine.anatomical_structurePhenotypeLarvaC. elegansFemaleNetrinsProteoglycansSignal transductionSignal TransductionUNC-52Nerve Tissue ProteinsReceptors Cell SurfacePerlecanmacromolecular substancesBiologymedicineAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsGonadsGeneMolecular BiologyGrowth factorfungiMembrane ProteinsCell BiologyPerlecanReceptors Fibroblast Growth Factornervous systemMutationbiology.proteinProtein Tyrosine PhosphatasesDevelopmental BiologyDevelopmental biology
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Q289P mutation in the FGFR2 gene: first report in a patient with type 1 Pfeiffer syndrome.

2008

When normal development and growth of the calvarial sutures is disrupted, craniosynostosis (premature calvarial suture fusion) may result. Classical craniosynostosis syndromes are autosomal dominant traits and include Apert, Pfeiffer, Crouzon, Jackson-Weiss, and Saethre-Chotzen syndromes. In these conditions, there is premature fusion of skull bones leading to an abnormal head shape, ocular hypertelorism with proptosis, and midface hypoplasia. It is known that mutations in the fibroblast growth factor receptors 1, 2, and 3 cause craniosynostosis. We report on a child with a clinically diagnosed Pfeiffer syndrome that shows the missense point mutation Q289P in exon 8 of the FGFR2 gene. This …

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyCraniosynostosisSettore MED/38 - Pediatria Generale E SpecialisticaHumansPoint MutationMedicineMissense mutationReceptor Fibroblast Growth Factor Type 2HypertelorismGeneticsFibrous jointbusiness.industryFibroblast growth factor receptor 2Craniofacial DysostosisInfantDysostosisExonsAcrocephalosyndactyliamedicine.diseaseSkullPhenotypemedicine.anatomical_structurePfeiffer - Crouzon - Apert - Craniosynostosis - Finger and toes abnormalities - Fibroblast growth factor receptorPediatrics Perinatology and Child HealthPfeiffer syndromeFemalemedicine.symptombusiness
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An asymmetric electrospun membrane for the controlled release of ciprofloxacin and FGF-2: Evaluation of antimicrobial and chemoattractant properties.

2021

Here, an asymmetric double-layer membrane has been designed and fabricated by electrospinning as a tool for a potential wound healing application. A hydrophobic layer has been produced by using a polyurethane-polycaprolactone (PU-PCL) copolymer and loaded with the antibacterial ciprofloxacin whereas an ion responsive hydrophilic layer has been produced by using an octyl derivative of gellan gum (GG-C8) and polyvinyl alcohol (PVA) and loaded with the growth factor FGF-2. This study investigated how the properties of this asymmetric membrane loaded with actives, were influenced by the ionotropic crosslinking of the hydrophilic layer. In particular, the treatment in DPBS and the crosslinking i…

Materials sciencePolyurethanesNanofibersBioengineeringmacromolecular substances02 engineering and technologyChemotaxis (FGF-2)Antimicrobial activity (CPX); Chemotaxis (FGF-2); Double layer electrospun membrane; Gellan gum alkyl-derivative; Polyurethanes010402 general chemistry01 natural sciencesPolyvinyl alcoholGellan gum alkyl-derivativeBiomaterialschemistry.chemical_compoundAnti-Infective AgentsCiprofloxacinCopolymerDouble layer electrospun membraneChemotactic Factorstechnology industry and agriculture021001 nanoscience & nanotechnologyAntimicrobialControlled releaseBandagesGellan gumElectrospinning0104 chemical sciencesAnti-Bacterial AgentsAntimicrobial activity (CPX)MembranechemistryMechanics of MaterialsSettore CHIM/09 - Farmaceutico Tecnologico ApplicativoDelayed-Action PreparationsBiophysicsFibroblast Growth Factor 20210 nano-technologyLayer (electronics)Materials scienceengineering. C, Materials for biological applications
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Synthesis, Structural Elucidation, and Biological Evaluation of NSC12, an Orally Available Fibroblast Growth Factor (FGF) Ligand Trap for the Treatme…

2016

NSC12 is an orally available pan-FGF trap able to inhibit FGF2/FGFR interaction and endowed with promising antitumor activity. It was identified by virtual screening from a NCI small molecule library, but no data were available about its synthesis, stereochemistry, and physicochemical properties. We report here a synthetic route that allowed us to characterize and unambiguously identify the structure of the active compound by a combination of NMR spectroscopy and in silico conformational analysis. The synthetic protocol allowed us to sustain experiments aimed at assessing its therapeutic potential for the treatment of FGF-dependent lung cancers. A crucial step in the synthesis generated a c…

Models Molecular0301 basic medicineLung NeoplasmssynthesisFGF Lung cancer growth factor chemical characterization synthesisIn silicoAdministration OralAntineoplastic AgentsPharmacologyFibroblast growth factorMiceStructure-Activity Relationship03 medical and health sciences0302 clinical medicineIn vivoDrug DiscoveryTumor Cells CulturedAnimalsHumansFGFStructure–activity relationshipCell ProliferationDose-Response Relationship DrugMolecular Structurechemical characterizationCell growthChemistrygrowth factorLigand (biochemistry)Small moleculeCell biologyFibroblast Growth FactorsCholesterol030104 developmental biologyFibroblast growth factor receptor030220 oncology & carcinogenesisMolecular MedicineDrug Screening Assays AntitumorLung cancerJournal of Medicinal Chemistry
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