Search results for "FIBROBLAST"

showing 10 items of 667 documents

SNAT2 silencing prevents the osmotic induction of transport system A and hinders cell recovery from hypertonic stress.

2005

AbstractUnder hypertonic conditions the induction of SLC38A2/SNAT2 leads to the stimulation of transport system A and to the increase in the cell content of amino acids. In hypertonically stressed human fibroblasts transfection with two siRNAs for SNAT2 suppressed the increase in SNAT2 mRNA and the stimulation of system A transport activity. Under the same condition, the expansion of the intracellular amino acid pool was significantly lowered and cell volume recovery markedly delayed. It is concluded that the up-regulation of SNAT2 is essential for the rapid restoration of cell volume after hypertonic stress.

Small interfering RNAmedicine.medical_specialtyAmino Acid Transport System AGlutamineCellBiophysicsStimulationBiologyTransfectionBiochemistryStructural BiologyOsmotic PressureCell volumeInternal medicineGeneticsmedicineHumansRNA MessengerAmino AcidsRNA Small InterferingMolecular BiologyCell Sizechemistry.chemical_classificationSaline Solution HypertonicCell BiologyFibroblastsAmino acidCell biologyUp-RegulationGlutaminemedicine.anatomical_structureEndocrinologychemistryHypertonic StresssiRNATonicityRNA InterferenceIntracellularFEBS letters
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CEND1 and NEUROGENIN2 Reprogram Mouse Astrocytes and Embryonic Fibroblasts to Induced Neural Precursors and Differentiated Neurons

2015

Summary Recent studies demonstrate that astroglia from non-neurogenic brain regions can be reprogrammed into functional neurons through forced expression of neurogenic factors. Here we explored the effect of CEND1 and NEUROG2 on reprogramming of mouse cortical astrocytes and embryonic fibroblasts. Forced expression of CEND1, NEUROG2, or both resulted in acquisition of induced neuronal cells expressing subtype-specific markers, while long-term live-cell imaging highlighted the existence of two different modes of neuronal trans-differentiation. Of note, a subpopulation of CEND1 and NEUROG2 double-transduced astrocytes formed spheres exhibiting neural stem cell properties. mRNA and protein exp…

Somatic cellCellular differentiationNerve Tissue ProteinsEndogenyBiologyBiochemistryArticleMiceNeural Stem CellsBasic Helix-Loop-Helix Transcription FactorsGeneticsAnimalslcsh:QH301-705.5NeuronsGene knockdownMessenger RNAlcsh:R5-920Membrane ProteinsCell DifferentiationCell BiologyFibroblastsCellular ReprogrammingEmbryo MammalianEmbryonic stem cellNeural stem cellCell biologylcsh:Biology (General)Astrocytesembryonic structureslcsh:Medicine (General)ReprogrammingDevelopmental BiologyStem Cell Reports
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Recovery of human fibroblasts from attack by the pore-forming alpha-toxin of Staphylococcus aureus.

1994

When applied at low concentrations (10 micrograms/ml), staphylococcal alpha-toxin generates a small channel in keratinocyte and lymphocyte membranes that permits selective transmembrane flux of monovalent ions. Here we show that a moderate concentration (1-50 micrograms/ml) of alpha-toxin similarly produces a small pore in membranes of human fibroblasts. This process leads to rapid leakage of K+ and to a drop in cellular ATP to 10-20% of normal levels in 2 h. In the presence of medium supplemented with serum and at pH 7.4, the cells are able to recover from toxin attack, so that normal levels of K+ and ATP are reached after 6-8 h at 37 degrees C. The repair process is dependent on the prese…

Staphylococcus aureusLymphocyteBacterial ToxinsBiologymedicine.disease_causeMicrobiologyOuabainIon ChannelsCell LineHemolysin ProteinsAdenosine TriphosphatemedicineHumansFibroblastOuabainToxinCell MembraneHemolysinFibroblastsTransmembrane proteinCulture MediaKineticsInfectious Diseasesmedicine.anatomical_structureMembraneBiochemistryBiophysicsPotassiumStreptolysinmedicine.drugMicrobial pathogenesis
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Polysaccharide/polyaminoacid composite scaffolds for modified DNA release.

2009

Abstract In this work composite polymeric films or sponges, based on hyaluronic acid (HA) covalently crosslinked with α,β-poly(N-2-hydroxyethyl)(2-aminoethylcarbamate)- d , l -aspartamide (PE), have been prepared and characterized as local gene delivery systems. In particular, HA/PE scaffolds have been loaded with PE/DNA interpolyelectrolyte complexes, employing PE as a macromolecular crosslinker for HA and as a non-viral vector for DNA. In vitro studies showed that HA/PE films and sponges have high compatibility with human dermal fibroblasts and they give a sustained DNA release, whose trend can be easily tailored by varying the crosslinking ratio between HA and PE. Electrophoresis analysi…

StereochemistryMelanoma ExperimentalPharmaceutical ScienceHyaluronoglucosaminidaseElectrophoretic Mobility Shift Assaymacromolecular substancesBiologyGene deliveryTransfectionchemistry.chemical_compoundMiceTissue engineeringHyaluronic acidPolyaminesCOMPOSITE SCAFFOLD SCAFFOLD AMINOACID DNA RELEASE.AnimalsHumansHyaluronic AcidAspartameCells CulturedMolecular StructureGenetic transfertechnology industry and agricultureBiological TransportTransfectionDNAFibroblastsIn vitroKineticsCross-Linking ReagentschemistrySolubilitySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoNucleic Acid ConformationDNAMacromoleculeNuclear chemistryInternational journal of pharmaceutics
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Inhibition of B2 receptor internalization delays its dephosphorylation

1997

SucroseReceptor Bradykinin B2Immunoprecipitationmedia_common.quotation_subjectBradykininBradykininCell LineDephosphorylationRadioligand Assaychemistry.chemical_compoundOkadaic AcidConcanavalin APhosphoprotein PhosphatasesHumansEnzyme InhibitorsPhosphorylationInternalizationOxazolesBradykinin Receptor AntagonistsSkinmedia_commonPharmacologyChemistryReceptors BradykininOkadaic acidFibroblastsPrecipitinPrecipitin TestsRadioligand AssayBiochemistryCantharidinIrritantsAutoradiographyPhosphorylationElectrophoresis Polyacrylamide GelMarine ToxinsImmunopharmacology
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Cytokines and growth factors in wound drainage fluid from patients undergoing incisional hernia repair

2006

Knowing the dynamics of growth factor and cytokine secretion within the site of a surgical operation is important, as they play a crucial role in the pathophysiology of wound healing and are a target for modifying the repair response. The aim of this study was to evaluate the production of several cytokines and growth factors in the drainage wound fluid from patients undergoing incisional hernia repair: namely, interleukin (IL)-6, IL-10, IL-1alpha, IL-1 ra, interferon-gamma, vascular endothelial growth factors and basic fibroblast growth factor. Ten female patients with abdominal midline incisional hernia undergoing surgical repair were included in this study. In all cases, a closed-suction…

Surgical repairmedicine.medical_specialtybusiness.industryIncisional herniaGrowth factormedicine.medical_treatmentBasic fibroblast growth factorSurgical woundDermatologymedicine.diseaseSurgerychemistry.chemical_compoundCytokinechemistryAnesthesiamedicineSurgeryCytokine secretionWound healingbusinessWound Repair and Regeneration
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Topotecan triggers apoptosis in p53-deficient cells by forcing degradation of XIAP and survivin thereby activating caspase-3-mediated Bid cleavage.

2009

The topoisomerase I inhibitor topotecan (TPT) is used in the therapy of different tumors including high-grade gliomas. We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I. Here, we show that p53-deficient (p53(-/-)) fibroblasts undergo excessive mitochondrial apoptosis featuring H2AX phosphorylation, Bcl-x(L) decline, cytochrome c release, caspase-9/-3/-2 activation, and cleavage of Bid. In wt and apaf-1(-/-) cells, caspase-2 did not become activated and Bid was not cleaved. In addition, p53(-/-) cells cotreated with TPT and caspase-3 inhibitor showed neither caspase-2 acti…

SurvivinBlotting WesternDown-RegulationCaspase 3ApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyTopoisomerase-I InhibitorInhibitor of apoptosisTransfectionInhibitor of Apoptosis ProteinsHistonesMiceCell Line TumorSurvivinAnimalsHumansPhosphorylationRNA Small InterferingPharmacologyMice KnockoutCaspase 3Caspase 2TransfectionFibroblastsFlow CytometryMolecular biologyXIAPMice Inbred C57BLRepressor ProteinsApoptotic Protease-Activating Factor 1ApoptosisCancer researchMolecular MedicineApoptosomeTopoisomerase I InhibitorsTumor Suppressor Protein p53TopotecanMicrotubule-Associated ProteinsBH3 Interacting Domain Death Agonist ProteinThe Journal of pharmacology and experimental therapeutics
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HNRNPR Variants that Impair Homeobox Gene Expression Drive Developmental Disorders in Humans

2019

The heterogeneous nuclear ribonucleoprotein (HNRNP) genes code for a set of RNA-binding proteins that function primarily in the spliceosome C complex. Pathogenic variants in these genes can drive neurodegeneration, through a mechanism involving excessive stress-granule formation, or developmental defects, through mechanisms that are not known. Here, we report four unrelated individuals who have truncating or missense variants in the same C-terminal region of hnRNPR and who have multisystem developmental defects including abnormalities of the brain and skeleton, dysmorphic facies, brachydactyly, seizures, and hypoplastic external genitalia. We further identified in the literature a fifth ind…

TBX1MaleSpliceosomeHeterogeneous nuclear ribonucleoproteinDevelopmental DisabilitiesRNA SplicingBiologyHeterogeneous-Nuclear Ribonucleoproteins/geneticsHeterogeneous-Nuclear RibonucleoproteinsArticleWhole Exome Sequencing03 medical and health sciences0302 clinical medicineExome SequencingGeneticsHumansGenes Homeobox/geneticsPreschoolHox geneChildGeneTranscription factorGenetics (clinical)RNA Splicing/genetics030304 developmental biologyGeneticsFibroblasts/metabolism0303 health sciencesHomeobox/geneticsGenes HomeoboxInfantFibroblastsOxidative StressPhenotypeGenesDevelopmental Disabilities/etiologyGene Expression RegulationChild PreschoolRNA splicingMutationHomeoboxFemale030217 neurology & neurosurgery
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The role of the fibronectin synergy site in skin wound healing

2022

Upon skin barrier disruption, complex cellular and molecular events are activated to repair the damage and restore skin integrity. In adulthood, the outcome of this process can result in scarring and fibrosis, whereas complete tissue regeneration is observed in fetal wounds and wounds in lower vertebrates and invertebrates .Although there is abundant literature about the factors and mechanisms that determine the endpoint of either scarring/fibrosis or regeneration after tissue injury, the process is still poorly understood. After cutaneous injury, fibronectin (FN) is instantly released and deposited by cells, and represents a major ECM component in all stages of the wound healing process. F…

TGF-β1myofibroblastsUNESCO::CIENCIAS DE LA VIDAsynergy sitewound healingα5β1 integrinfibronecin
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Regulation of B cell homeostasis and activation by the tumor suppressor gene CYLD

2007

B cell homeostasis is regulated by multiple signaling processes, including nuclear factor-kappaB (NF-kappaB), BAFF-, and B cell receptor signaling. Conditional disruption of genes involved in these pathways has shed light on the mechanisms governing signaling from the cell surface to the nucleus. We describe a novel mouse strain that expresses solely and excessively a naturally occurring splice variant of CYLD (CYLD(ex7/8) mice), which is a deubiquitinating enzyme that is integral to NF-kappaB signaling. This shorter CYLD protein lacks the TRAF2 and NEMO binding sites present in full-length CYLD. A dramatic expansion of mature B lymphocyte populations in all peripheral lymphoid organs occur…

TRAF2Tumor suppressor geneImmunologyCellBiologyArticleDeubiquitinating Enzyme CYLDMiceB cell homeostasismedicineAnimalsHomeostasisImmunology and AllergyB-cell activating factorEmbryonic Stem CellsSequence DeletionB-LymphocytesRELBGenetic VariationExonsArticlesFibroblastsDeubiquitinating Enzyme CYLDAlternative SplicingCysteine Endopeptidasesmedicine.anatomical_structureProtein BiosynthesisCancer researchSignal transductionSignal TransductionJournal of Experimental Medicine
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