Search results for "Umbilical"

showing 10 items of 331 documents

Relative contribution of different l-arginine sources to the substrate supply of endothelial nitric oxide synthase

2011

In certain cases of endothelial dysfunction l-arginine becomes rate-limiting for NO synthesis in spite of sufficiently high plasma concentrations of the amino acid. To better understand this phenomenon, we investigated routes of substrate supply to endothelial nitric oxide synthase (eNOS). Our previous data with human umbilical vein (HUVEC) and EA.hy.926 endothelial cells demonstrated that eNOS can obtain its substrate from the conversion of l-citrulline to l-arginine and from protein breakdown. In the present study, we determined the quantitative contribution of proteasomal and lysosomal protein degradation and investigated to what extent extracellular peptides and l-citrulline can provide…

Proteasome Endopeptidase ComplexNitric Oxide Synthase Type IIIArginineEndotheliumLeupeptinsPeptideArginineNitric OxideUmbilical veinCell LineGenes ReporterEnosLysosomeHuman Umbilical Vein Endothelial CellsmedicineExtracellularHumansHistidineProtease InhibitorsMolecular BiologyChromatography High Pressure LiquidHistidinechemistry.chemical_classificationbiologyMembrane Transport ProteinsBiological TransportChloroquineDipeptidesAtherosclerosisbiology.organism_classificationmedicine.anatomical_structureBiochemistrychemistryProteolysisCitrullineEndothelium VascularLysosomesCardiology and Cardiovascular MedicineOligopeptidesJournal of Molecular and Cellular Cardiology
researchProduct

Exosomes from metastatic cancer cells transfer amoeboid phenotype to non-metastatic cells and increase endothelial permeability: their emerging role …

2017

AbstractThe goal of this study was to understand if exosomes derived from high-metastatic cells may influence the behavior of less aggressive cancer cells and the properties of the endothelium. We found that metastatic colon cancer cells are able to transfer their amoeboid phenotype to isogenic primary cancer cells through exosomes, and that this morphological transition is associated with the acquisition of a more aggressive behavior. Moreover, exosomes from the metastatic line (SW620Exos) exhibited higher ability to cause endothelial hyperpermeability than exosomes from the non metastatic line (SW480Exos). SWATH-based quantitative proteomic analysis highlighted that SW620Exos are signific…

Proteomics0301 basic medicineRHOAEndotheliummetastatic cancer cellScienceCell PlasticityContext (language use)ExosomesArticlePermeability03 medical and health sciences0302 clinical medicineSettore BIO/13 - Biologia ApplicataCell Line Tumormetastatic cancer cells; Exosomes; tumor heterogeneitytumor heterogeneityHuman Umbilical Vein Endothelial CellsmedicineHumansEndotheliumrho-Associated KinasesMultidisciplinarybiologyQThrombinRPhenotypeMicrovesicles3. Good healthCell biologyEndothelial stem cellExosomePhenotype030104 developmental biologymedicine.anatomical_structureTumor progression030220 oncology & carcinogenesisColonic NeoplasmsCancer cellbiology.proteinMedicinerhoA GTP-Binding ProteinSignal Transduction
researchProduct

Proteomic Profiling of Secreted Proteins for the Hematopoietic Support of Interleukin-Stimulated Human Umbilical Vein Endothelial Cells

2013

Human umbilical cord vein endothelial cells (HUVECs) secrete a number of factors that greatly impact the proliferation and differentiation of hematopoietic stem and progenitor cells (HSPCs). These factors remain largely unknown. Here, we report on the most comprehensive proteomic profiling of the HUVEC secretome and identified 827 different secreted proteins. Two hundred and thirty-one proteins were found in all conditions, whereas 369 proteins were identified only under proinflammatory conditions following IL-1β, IL-3, and IL-6 stimulation. Thirteen proteins including complement factor b (CFb) were identified only under IL-1β and IL-3 conditions and may potentially represent HSPC prolifer…

ProteomicsSpectrometry Mass Electrospray IonizationInterleukin-1betaBiomedical EngineeringComplement C5blcsh:MedicineAntigens CD34BiologyComplement factor BUmbilical veinProinflammatory cytokineHuman Umbilical Vein Endothelial CellsHumansProgenitor cellCell ProliferationTransplantationInterleukin-6lcsh:RAntibodies MonoclonalComputational BiologyInterleukinComplement System ProteinsCell BiologyFlow CytometryHematopoietic Stem CellsMolecular biologyUp-RegulationComplement systemHaematopoiesisElectrophoresis Polyacrylamide GelInterleukin-3Stem cellPeptidesCell Transplantation
researchProduct

C7 is expressed on endothelial cells as a trap for the assembling terminal complement complex and may exert anti-inflammatory function.

2009

AbstractWe describe a novel localization of C7 as a membrane-bound molecule on endothelial cells (ECs). Data obtained by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE), Western blot analysis, Northern blot analysis, and mass spectrometry revealed that membrane-associated C7 (mC7) was indistinguishable from soluble C7 and was associated with vimentin on the cell surface. mC7 interacted with the other late complement components to form membrane-bound TCC (mTCC). Unlike the soluble SC5b-9, mTCC failed to stimulate ECs to express adhesion molecules, to secrete IL-8, and to induce albumin leakage through a monolayer of ECs, and more importantly protected ECs from the proinf…

ProteomicsVasculitisUmbilical VeinsVasculitiImmunologyComplementComplement; C7; endothelial cells; inflammationComplement Membrane Attack ComplexBiologyBiochemistryProinflammatory cytokineWestern blotmedicineHumansVimentinC7Interleukin 8Northern blotRNA MessengerMembrane ProteinCells CulturedGel electrophoresisEndothelial Cellmedicine.diagnostic_testCell adhesion moleculeComplement; endothelial cells; inflammationInterleukin-8Endothelial CellsMembrane ProteinsProteomicUmbilical VeinHematologyCell BiologyMolecular biologyComplement C7Endothelial stem cellCells Cultured; Complement C7; Complement Membrane Attack Complex; Endothelial Cells; Humans; Interleukin-8; Membrane Proteins; Proteomics; RNA Messenger; Umbilical Veins; Vasculitis; Vimentin; Hematology; Biochemistry; Cell Biology; Immunologyinflammationendothelial cellComplement membrane attack complexHuman
researchProduct

Modulation of endotoxin-induced neutrophil transendothelial migration by alveolar epithelium in a defined bilayer model.

2006

Within the alveolus, epithelial cells, due to their close association with endothelial cells, can potentially influence endothelial cell responsiveness during inflammation and their interaction with leukocytes. To investigate this, three lung epithelial cell lines (A549, Calu-3, or NCI-H441) were grown with endothelium on opposing surfaces of Transwell filters and the formation and stability of bilayers was rigorously evaluated. All epithelial lines disrupted endothelial monolayer formation on filters with 3- or 5-microm pores by breaching the filter, and this occurred regardless of seeding density, matrix composition, or duration of culture. Endothelial disruption was not detectable by ele…

Pulmonary and Respiratory MedicineLipopolysaccharidesEndotheliumNeutrophilsClinical BiochemistryInflammationEnzyme-Linked Immunosorbent AssayBiologyUmbilical veinCell LineCell MovementmedicineHumansMolecular BiologyA549 cellLung alveolusMicropore FiltersEpitheliumCoculture TechniquesCell biologyEndothelial stem cellPulmonary Alveolimedicine.anatomical_structureCell cultureImmunologyEndothelium Vascularmedicine.symptomExperimental lung research
researchProduct

GM-CSF expression by human lung microvascular endothelial cells: in vitro and in vivo findings.

2002

Recently, many findings indicate that granulocyte-macrophage colony-stimulating factor (GM-CSF) plays an important role in the pathogenesis of acute and chronic lung diseases. In the present paper, the production of this cytokine in human pulmonary microvascular endothelial cells (HPMEC) is investigated. In an in vitro study, quiescent HPMEC did not express GM-CSF, either at the transcriptional or at the protein level. After activation for 4 h with tumor necrosis factor (TNF)-α (30/300 U/ml), lipopolysaccharide (LPS; 0.1/1 μg/ml), or interleukin (IL)-1β (100 U/ml), a significant release of GM-CSF was measured by enzyme-linked immunosorbent assay, with a time-dependent increase over 72 h. IL…

Pulmonary and Respiratory MedicinePathologymedicine.medical_specialtyPulmonary CirculationUmbilical VeinsEndotheliumPhysiologymedicine.medical_treatmentHemangiosarcomaEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesPathogenesisIn vivoPhysiology (medical)medicineHumansCells CulturedLungbusiness.industryReverse Transcriptase Polymerase Chain ReactionMicrocirculationRespiratory diseaseGranulocyte-Macrophage Colony-Stimulating FactorCell Biologymedicine.diseaseImmunohistochemistryEndothelial stem cellGranulocyte macrophage colony-stimulating factorCytokinemedicine.anatomical_structureEndothelium Vascularbusinessmedicine.drugAmerican journal of physiology. Lung cellular and molecular physiology
researchProduct

Induction of stress proteins in human endothelial cells by heavy metal ions and heat shock.

1999

In the present study, we compared the induction of heat shock proteins (HSPs) by heat and heavy metal ions in three different endothelial cell types, namely, human umbilical vein endothelial cells, human pulmonary microvascular endothelial cells, and the cell line EA.hy 926. Our results show that especially Zn2+and Cd2+are inducers of 70-kDa (HSP70), 60-kDa (HSP60), 32-kDa (HSP32), and 27-kDa (HSP27) HSPs. The strength of inducibility is specific for each HSP. Ni2+and Co2+only show an inducible effect at very high concentrations, that is, in the clearly cytotoxic range. Furthermore, we investigated the time course of HSP expression and the involvement of heat shock factor-1. Our study demon…

Pulmonary and Respiratory MedicineUmbilical VeinsPhysiologyMetal ions in aqueous solutionBlotting WesternGene ExpressionBiologyUmbilical veinPhysiology (medical)Heat shock proteinMetals HeavyGene expressionmedicineHumansHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsRNA MessengerFluorescent Antibody Technique IndirectCells CulturedHeat-Shock ProteinsCell BiologyChaperonin 60Endothelial stem cellmedicine.anatomical_structureCell cultureShock (circulatory)ImmunologyBiophysicsEndothelium Vascularmedicine.symptomHeat-Shock ResponseBlood vesselThe American journal of physiology
researchProduct

Rho protein inactivation induced apoptosis of cultured human endothelial cells.

2002

Small GTP-binding Rho GTPases regulate important signaling pathways in endothelial cells, but little is known about their role in endothelial cell apoptosis. Clostridial cytotoxins specifically inactivate GTPases by glucosylation [ Clostridium difficile toxin B-10463 (TcdB-10463), C. difficile toxin B-1470 (TcdB-1470)] or ADP ribosylation ( C. botulinum C3 toxin). Exposure of human umbilical cord vein endothelial cells (HUVEC) to TcdB-10463, which inhibits RhoA/Rac1/Cdc42, or to C3 toxin, which inhibits RhoA, -B, -C, resulted in apoptosis, whereas inactivation of Rac1/Cdc42 with TcdB-1470 was without effect, suggesting that Rho inhibition was responsible for endothelial apoptosis. Disruptio…

Pulmonary and Respiratory Medicinerac1 GTP-Binding Proteinrho GTP-Binding ProteinsProgrammed cell deathUmbilical VeinsEndotheliumPhysiologyBacterial ToxinsCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBcl-2-associated X proteinBacterial ProteinsPhysiology (medical)Proto-Oncogene ProteinsmedicineCyclic AMPIn Situ Nick-End LabelingHumanscdc42 GTP-Binding ProteinCells Culturedbcl-2-Associated X ProteinAdenosine Diphosphate RibosebiologyCaspase 3Intracellular Signaling Peptides and ProteinsCell BiologyCaspase 9Cell biologyNeoplasm ProteinsEndothelial stem cellmedicine.anatomical_structureCdc42 GTP-Binding ProteinProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisCaspasesbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinEndothelium VascularSignal transductionCarrier ProteinsrhoA GTP-Binding ProteinBH3 Interacting Domain Death Agonist ProteinSignal TransductionAmerican journal of physiology. Lung cellular and molecular physiology
researchProduct

Inhibition of VEGF expression through blockade of Hif1a and STAT3 signalling mediates the anti-angiogenic effect of melatonin in HepG2 liver cancer c…

2013

Background: Hepatocellular carcinoma (HCC) growth relies on angiogenesis via vascular endothelial growth factor (VEGF) release. Hypoxia within tumour environment leads to intracellular stabilisation of hypoxia inducible factor 1 alpha (Hif1α) and signal transducer and activator of transcription (STAT3). Melatonin induces apoptosis in HCC, and shows anti-angiogenic features in several tumours. In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate the anti-angiogenic effects of melatonin. Methods: HepG2 cells were treated with melatonin under normoxic or CoCl2-induced hypoxia. Gene expression was analysed by RT–qPCR and western blot. Melatonin-induced anti-…

STAT3 Transcription FactorTranscriptional ActivationVascular Endothelial Growth Factor ACancer ResearchCarcinoma HepatocellularTranscription GeneticAngiogenesisAngiogenesis InhibitorsApoptosismelatoninP300-CBP Transcription FactorsHif1αBiologyMelatoninSTAT3chemistry.chemical_compoundHypoxia-Inducible Factor 1-AlphamedicineHuman Umbilical Vein Endothelial CellsHumansp300-CBP Transcription FactorsSTAT3Promoter Regions GeneticTube formationNeovascularization PathologicLiver NeoplasmsCobaltHep G2 Cellshepatocellular carcinomaHypoxia-Inducible Factor 1 alpha SubunitVEGFCell Hypoxiadigestive system diseasesCyclic S-OxidesVascular endothelial growth factorGene Expression Regulation NeoplasticVascular endothelial growth factor AOncologychemistryCancer researchbiology.proteinTranslational Therapeuticsmedicine.drugSignal Transduction
researchProduct

The pre-vascularisation of a collagen-chondroitin sulphate scaffold using human amniotic fluid-derived stem cells to enhance and stabilise endothelia…

2015

Abstract A major problem in tissue engineering (TE) is graft failure in vivo due to core degradation in in vitro engineered constructs designed to regenerate thick tissues such as bone. The integration of constructs post-implantation relies on the rapid formation of functional vasculature. A recent approach to overcome core degradation focuses on the creation of cell-based, pre-engineered vasculature formed within the TE construct in vitro , prior to implantation in vivo . The primary objective of this study was to investigate whether an amniotic fluid-derived stem cell (AFSC)–human umbilical vein endothelial cell (HUVEC) co-culture could be used to engineer in vitro vasculature in a collag…

ScaffoldMaterials scienceBiomedical EngineeringNeovascularization PhysiologicBiochemistryUmbilical veinBiomaterialsTissue engineeringBlood vessel prosthesisIn vivoMaterials TestingHumansBone regenerationMolecular BiologyCells CulturedBioprosthesisTissue ScaffoldsStem CellsChondroitin SulfatesEndothelial CellsEquipment DesignGeneral MedicineAmniotic FluidBlood Vessel ProsthesisCapillariesCell biologyEquipment Failure AnalysisEndothelial stem cellCollagenStem cellStem Cell TransplantationBiotechnologyBiomedical engineeringActa Biomaterialia
researchProduct