Search results for " endothelial cells"

showing 10 items of 132 documents

Synthesis of a new class of pyrrolo[3,4-h]quinazolines with antimitotic activity

2014

Abstract A new series of pyrrolo[3,4- h ]quinazolines was conveniently prepared with a broad substitution pattern. A large number of derivatives was obtained and the cellular cytotoxicity was evaluated in vitro against 5 different human tumor cell lines with GI 50 values reaching the low micromolar level (1.3–19.8 μM). These compounds were able to induce cell death mainly by apoptosis through a mitochondrial dependent pathway. Selected compounds showed antimitotic activity and a reduction of tubulin polymerization in a concentration-dependent manner. Moreover, they showed anti-angiogenic properties since reduced in vitro endothelial cell migration and disrupted HUVEC capillary-like tube net…

Programmed cell deathMitosisAntiproliferative activityCell Line TumorDrug DiscoveryHuman Umbilical Vein Endothelial CellsPiHumansTubulin polymerizationPyrrolesPyrrolo[3Cell-mediated cytotoxicityPyrrolo[34-h]quinazolines Antiproliferative activity Antimitotic activity Tubulin polymerization Vascular disrupting activityTubulin polymerizationVascular disrupting activityPharmacologyMatrigelCell Death4-h]quinazolinesChemistryAntimitotic activityOrganic ChemistryGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaMitochondriaEndothelial stem cellBiochemistryCell cultureApoptosisPyrrolo[3; 4-h]quinazolines; Antiproliferative activity; Antimitotic activity; Tubulin polymerization; Vascular disrupting activityQuinazolinesLysosomes
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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
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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
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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
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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
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Circulating haemopoietic and endothelial progenitor cells are decreased in COPD

2006

Circulating CD34+ cells are haemopoietic progenitors that may play a role in tissue repair. No data are available on circulating progenitors in chronic obstructive pulmonary disease (COPD). Circulating CD34+ cells were studied in 18 patients with moderate-to-severe COPD (age: mean+/-sd 68+/-8 yrs; forced expiratory volume in one second: 48+/-12% predicted) and 12 controls, at rest and after endurance exercise. Plasma concentrations of haematopoietic growth factors (FMS-like tyrosine kinase 3 (Flt3) ligand, kit ligand), markers of hypoxia (vascular endothelial growth factor (VEGF)) and stimulators of angiogenesis (VEGF, hepatocyte growth factor (HGF)) and markers of systemic inflammation (tu…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyAngiogenesisCD34Antigens CD34cd34Settore MED/10 - Malattie Dell'Apparato RespiratorioSettore BIO/09 - Fisiologiachronic obstructive pulmonary diseaseimmunologyPulmonary Disease Chronic Obstructivecd34+ cellscd34+cellschemistry.chemical_compoundantigensbloodstem cellsInternal medicinegrowth factorsmiddle agedMedicineProgenitor cellhumansCD34+ cells chronic obstructive pulmonary disease exercise growth factors hypoxiacell countpulmonary diseaseCOPDchronic obstructiveexercisehypoxiabusiness.industryaged; antigens; blood; cd34; cd34+ cells; cd34+cells; cell count; chronic obstructive; chronic obstructive pulmonary disease; endothelial cells; exercise; growth factors; hematopoietic stem cells; humans; hypoxia; immunology; middle aged; pulmonary disease; stem cellsHypoxia (medical)medicine.diseaseendothelial cellshematopoietic stem cellsEndothelial stem cellVascular endothelial growth factoragedEndocrinologychemistryHepatocyte growth factormedicine.symptombusinessmedicine.drugEuropean Respiratory Journal
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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
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Can Be miR-126-3p a Biomarker of Premature Aging? An Ex Vivo and In Vitro Study in Fabry Disease

2021

Fabry disease (FD) is a lysosomal storage disorder (LSD) characterized by lysosomal accumulation of glycosphingolipids in a wide variety of cytotypes, including endothelial cells (ECs). FD patients experience a significantly reduced life expectancy compared to the general population

SenescencePremature agingAdultMalesenescenceAdolescentPopulationsmall extracellular vesiclesUmbilical veinArticleAndrologyExtracellular VesiclesYoung AdultHUVECIn vivosmall extracellular vesicleHuman Umbilical Vein Endothelial CellsmiR-126-3pMedicineHumanseducationlcsh:QH301-705.5Cellular SenescenceAgedAged 80 and overSettore MED/04 - Patologia Generaleeducation.field_of_studySphingolipidsFabry diseasemicroRNAbusiness.industryagingAging PrematureGeneral MedicineMiddle Agedmedicine.diseaseFabry diseaseendothelial cellsMicroRNAslcsh:Biology (General)endothelial cellBiomarker (medicine)NanoparticlesFemaleGlycolipidsbusinessReactive Oxygen SpeciesEx vivoBiomarkersCells
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Shedding of Membrane Vesicles Mediates Fibroblast Growth Factor-2 Release from Cells

2003

Fibroblast growth factor-2 (FGF-2), a polypeptide with regulatory activity on cell growth and differentiation, lacks a conventional secretory signal sequence, and its mechanism of release from cells remains unclear. We characterized the role of extracellular vesicle shedding in FGF-2 release. Viable cells released membrane vesicles in the presence of serum. However, in serum-free medium vesicle shedding was dramatically down-regulated, and the cells did not release FGF-2 activity into their conditioned medium. Addition of serum to serum-starved cells rapidly induced intracellular FGF-2 clustering under the plasma membrane and into granules that colocalized with patches of the cell membrane …

SerumFGF-2 extracellular vesiclesBiologyFibroblast growth factorBiochemistryCulture Media Serum-FreeSettore MED/13 - EndocrinologiaCell Line; Tumor; Endothelial Cells; Fibroblast Growth Factor 2; Secretory VesiclesCell LineCell membraneSettore BIO/13 - Biologia ApplicataCell Line TumorSettore BIO/10 - BiochimicamedicineHumansProtein IsoformsFibroblastMolecular BiologyTumorSecretory VesiclesVesicleCell MembraneEndothelial CellsCell BiologyExtracellular vesicleSecretory VesicleCell biologyKineticsmedicine.anatomical_structureMicroscopy FluorescenceCell cultureFibroblast Growth Factor 2IntracellularJournal of Biological Chemistry
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Oxidative stress-driven expression of myeloperoxidase in endothelial cells results in accumulation of markers of oxidative and nitrosative stress in …

2009

Endothelial cells (ECs), are able to manage with higher concentrations of ROS as well as reactive nitrogen species, respect to the other cell types. The unbalance between oxidizing species and antioxidant cellular defences has been implicated in the pathogenesis of cardiovascular diseases. While the role of MPO in the oxidative burst is well established, the effects of this enzyme on endothelial biology have only recently come to light. MPO can interact with endothelial –derived NO causing its depletion and favouring its conversion to nitrogen dioxide radical, a compound responsible of protein nitration generating 3-nitrotyrosine. Moreover, MPO is the only enzyme capable to form hypoclorous…

Settore BIO/16 - Anatomia Umanamyeloperoxidase endothelial cells endocardium oxidative stress nitrosative stress hydrogen peroxide 3-chlorotyrosine 3-nitrotyrosine
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