Search results for " Umbilical"

showing 10 items of 156 documents

Structure and closure mechanism of the human umbilical artery

1978

The structure of the fully-patent umbilical artery and rearrangement of its structural elements with postnatal closure were examined in 10 centimeter long umbilical cord segments which were double-clamped at different time intervals after delivery. The fully-patent umbilical artery consists of two main layers: an outer layer of circularly arranged smooth muscle cells and an inner layer which shows rather irregularly and loosely arranged cells embedded in abundant metachromatic ground substance. No predominantly longitudinal arrangements of cells and fibers reported by earlier investigators could be identified in the inner layer. Closure of the umbilical arteries is initiated by numerous loc…

MyofilamentGround substanceLumen (anatomy)Cell DifferentiationMuscle SmoothUmbilical arteryAnatomyBiologyUmbilical ArteriesLong umbilical cordlaw.inventionMicroscopy Electronmedicine.anatomical_structurelawmedicine.arteryPediatrics Perinatology and Child HealthmedicineHumansMyocyteElectron microscopeBlood vesselEuropean Journal of Pediatrics
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Polymeric Selectin Ligands Mimicking Complex Carbohydrates: From Selectin Binders to Modifiers of Macrophage Migration

2016

Novel polymeric cell adhesion inhibitors were developed in which the selectin tetrasaccharide sialyl-LewisX (SLeX ) is multivalently presented on a biocompatible poly(2-hydroxypropyl)methacrylamide (PHPMA) backbone either alone (P1) or in combination with O-sulfated tyramine side chains (P2). For comparison, corresponding polymeric glycomimetics were prepared in which the crucial "single carbohydrate" substructures fucose, galactose, and sialic acid side chains were randomly linked to the PHPMA backbone (P3 or P4 (O-sulfated tyramine)). All polymers have an identical degree of polymerization, as they are derived from the same precursor polymer. Binding assays to selectins, to activated endo…

OligosaccharidesTyramine02 engineering and technologyLigands010402 general chemistry01 natural sciencesCatalysisFucoseInhibitory Concentration 50chemistry.chemical_compoundPolymethacrylic AcidsCell MovementHuman Umbilical Vein Endothelial CellsSide chainHumansTetrasaccharideMethacrylamideSialyl Lewis X AntigenCell adhesionCells CulturedMacrophagesGeneral ChemistrySurface Plasmon ResonanceFlow Cytometry021001 nanoscience & nanotechnologyIn vitro0104 chemical sciencesSialic acidMicroscopy Fluorescence MultiphotonNanomedicinechemistryBiochemistrySelectins0210 nano-technologySelectinAngewandte Chemie International Edition
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C1q as a novel player in angiogenesis with therapeutic implication in wound healing

2014

We have previously shown that C1q is expressed on endothelial cells (ECs) of newly formed decidual tissue. Here we demonstrate that C1q is deposited in wound-healing skin in the absence of C4 and C3 and that C1q mRNA is locally expressed as revealed by real-time PCR and in situ hybridization. C1q was found to induce permeability of the EC monolayer, to stimulate EC proliferation and migration, and to promote tube formation and sprouting of new vessels in a rat aortic ring assay. Using a murine model of wound healing we observed that vessel formation was defective in C1qa(-/-) mice and was restored to normal after local application of C1q. The mean vessel density of wound-healing tissue and …

Pathologymedicine.medical_specialtycomplement C1qAngiogenesisImmunoblottingNeovascularization Physiologicchemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayIn situ hybridizationBiologyReal-Time Polymerase Chain ReactionangiogenesisMiceVasculogenesiscomplement; vasculogenesis; animal modelsimmune system diseasesmedicineangiogenesis; complement C1q; wound-healing; endothelial cellsHuman Umbilical Vein Endothelial CellsAnimalsHumanscomplementRats WistarIn Situ HybridizationCell ProliferationDNA PrimersTube formationMice KnockoutWound HealingMultidisciplinaryCell growthComplement C1qEndothelial CellsangiogenesivasculogenesiBiological Scienceswound-healingImmunohistochemistryanimal modelsendothelial cellsRatsMice Inbred C57BLReal-time polymerase chain reactionImmunohistochemistryWound healing
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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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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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