Search results for " endothelial cell"

showing 10 items of 177 documents

Dynamics of serum-induced endothelial cell apoptosis in patients with myocardial infarction

2013

In patients with ST-segment elevation myocardial infarction (STEMI) reperfused with primary coronary intervention (PCI), the dynamics of endothelial cell (EC) viability, apoptosis and necrosis and its relationship with the structural consequences on the left ventricle have not been addressed so far.In 20 STEMI patients, we incubated human umbilical vein endothelial cells (HUVECs) with serum drawn before reperfusion and subsequently afterwards (24, 96 h, 30 days). Viability, apoptosis and necrosis percentages were evaluated by flow cytometry. Values were compared with 12 age- and sex-matched control subjects with normal coronary arteries. Cardiac magnetic resonance (CMR) was performed during…

MaleSerummedicine.medical_specialtyNecrosisCell SurvivalClinical BiochemistryMyocardial InfarctionInfarctionApoptosisBiochemistryUmbilical veinNecrosisPercutaneous Coronary InterventionInternal medicineHuman Umbilical Vein Endothelial CellsmedicineHumanscardiovascular diseasesMyocardial infarctionAgedAged 80 and overbusiness.industryEndothelial CellsGeneral MedicineMiddle Agedmedicine.diseaseMagnetic Resonance ImagingEndothelial stem cellCardiac Imaging Techniquesmedicine.anatomical_structureVentricleApoptosisCase-Control StudiesConventional PCICardiologyFemalemedicine.symptombusinessEuropean Journal of Clinical Investigation
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Activation of the Constitutive Androstane Receptor Inhibits Leukocyte Adhesiveness to Dysfunctional Endothelium

2021

Leukocyte cell recruitment into the vascular subendothelium constitutes an early event in the atherogenic process. As the effect of the constitutive androstane receptor (CAR) on leukocyte recruitment and endothelial dysfunction is poorly understood, this study investigated whether the role of CAR activation can affect this response and the underlying mechanisms involved. Under physiological flow conditions, TNFα-induced endothelial adhesion of human leukocyte cells was concentration-dependently inhibited by preincubation of human umbilical arterial endothelial cells with the selective human CAR ligand CITCO. CAR agonism also prevented TNFα induced VCAM-1 expression, as well as MCP-1/CCL-2 a…

MaleSmall interfering RNAEndotheliumQH301-705.5Receptors Cytoplasmic and NuclearVascular Cell Adhesion Molecule-1Leukocyte RollingRetinoid X receptorArticleendothelial dysfunctionCatalysisInorganic ChemistryMiceConstitutive androstane receptorCell AdhesionHuman Umbilical Vein Endothelial CellsLeukocytesmedicineAnimalsHumansBiology (General)Physical and Theoretical ChemistryEndothelial dysfunctionQD1-999Molecular BiologySpectroscopyconstitutive androstane receptorTumor Necrosis Factor-alphaChemistryOrganic ChemistryNF-kappa BEndothelial Cellsleukocyte recruitmentGeneral Medicinemedicine.diseaseComputer Science ApplicationsCell biologyChemistrymedicine.anatomical_structureGene Expression RegulationTumor necrosis factor alphaIntravital microscopySignal TransductionInternational Journal of Molecular Sciences
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Dynamics of complement activation in aHUS and how to monitor eculizumab therapy.

2014

Atypical hemolytic-uremic syndrome (aHUS) is associated with genetic complement abnormalities/anti–complement factor H antibodies, which paved the way to treatment with eculizumab. We studied 44 aHUS patients and their relatives to (1) test new assays of complement activation, (2) verify whether such abnormality occurs also in unaffected mutation carriers, and (3) search for a tool for eculizumab titration. An abnormal circulating complement profile (low C3, high C5a, or SC5b-9) was found in 47% to 64% of patients, irrespective of disease phase. Acute aHUS serum, but not serum from remission, caused wider C3 and C5b-9 deposits than control serum on unstimulated human microvascular endotheli…

MaleTime FactorsClinical Trials and ObservationsComplement Membrane Attack Complexurologic and male genital diseasesBiochemistryGlomerulonephritisInside BLOOD Commentaryhemic and lymphatic diseasesMembranoproliferative glomerulonephritisMonoclonalHumanizedComplement ActivationAtypical Hemolytic Uremic SyndromeEndothelial CellHematologyRemission Inductionfood and beveragesHematologyComplement C3Eculizumabmedicine.anatomical_structureFactor HFemalecomplementaHUS eculizumabmedicine.drugMembranoproliferativeHumanmedicine.medical_specialtyEndotheliumMonitoringTime FactorGlomerulonephritis MembranoproliferativeImmunologyBiologyAntibodies Monoclonal HumanizedAntibodiesInternal medicineAtypical hemolytic uremic syndromemedicineHumansPhysiologicMonitoring PhysiologicAdenosine Diphosphate RiboseEndothelial CellsCell Biologymedicine.diseaseComplement systemImmunologyAdenosine Diphosphate Ribose; Antibodies Monoclonal Humanized; Atypical Hemolytic Uremic Syndrome; Complement Activation; Complement C3; Complement Membrane Attack Complex; Endothelial Cells; Female; Glomerulonephritis Membranoproliferative; Hemolytic-Uremic Syndrome; Humans; Male; Remission Induction; Time Factors; Monitoring Physiologic; Hematology; Biochemistry; Cell Biology; ImmunologyHemolytic-Uremic SyndromeComplement membrane attack complexBlood
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Association Between Platelet Endothelial Cellular Adhesion Molecule-1 Polymorphisms and Atherosclerosis: Results of a Study on Patients from Northern…

2010

Adhesion of circulating cells to the arterial surface is among the first detectable events in atherogenesis. Cellular adhesion molecules, expressed by the vascular endothelium and by circulating leukocytes, mediate cell recruitment and their transendothelial migration. Platelet endothelial cellular adhesion molecule-1 (PECAM-1), involved in this migration, has been associated with the development of atherosclerosis. Studies have investigated an association between coronary artery disease (CAD) and single-nucleotide polymorphisms (SNPs) located in functionally important domains of the PECAM-1 gene with inconsistent results. Thus, we have analyzed the distribution of V125L, N563S, and G670R S…

MaleUntranslated regionAgingGenotypeSingle-nucleotide polymorphismCoronary Artery DiseaseBiologyPolymorphism Single NucleotideCoronary artery diseaseGene FrequencymedicineHumansGenetic Predisposition to DiseasePlateletCell adhesionGeneAgedCell adhesion moleculeAdhesionMiddle AgedAtherosclerosismedicine.diseasePlatelet Endothelial Cell Adhesion Molecule-1ItalyCase-Control StudiesImmunologycardiovascular systemFemaleGeriatrics and GerontologyRejuvenation Research
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Vitamin D Receptor Activation Reduces Angiotensin-II–Induced Dissecting Abdominal Aortic Aneurysm in Apolipoprotein E–Knockout Mice

2015

Objective— Abdominal aortic aneurysm (AAA) is a vascular disorder characterized by chronic inflammation of the aortic wall. Low concentrations of vitamin D 3 are associated with AAA development; however, the potential direct effect of vitamin D 3 on AAA remains unknown. This study evaluates the effect of oral treatment with the vitamin D 3 receptor (VDR) ligand, calcitriol, on dissecting AAA induced by angiotensin-II (Ang-II) infusion in apoE −/− mice. Approach and Results— Oral treatment with calcitriol reduced Ang-II–induced dissecting AAA formation in apoE −/− mice, which was unrelated to systolic blood pressure or plasma cholesterol concentrations. Immunohistochemistry and reverse-tran…

MaleVascular Endothelial Growth Factor A0301 basic medicineDissecting Abdominal Aortic Aneurysm030204 cardiovascular system & hematologyLigandsCalcitriol receptorchemistry.chemical_compound0302 clinical medicineAorta AbdominalCells CulturedMice KnockoutAngiotensin IIVascular endothelial growth factorChemotaxis LeukocyteVascular endothelial growth factor APhenotypeMatrix Metalloproteinase 9Vitamin D3 ReceptorMatrix Metalloproteinase 2RNA Interferencelipids (amino acids peptides and proteins)ChemokinesMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineSignal Transductionmedicine.drugmedicine.medical_specialtyCalcitriolBiologyTransfectionProinflammatory cytokine03 medical and health sciencesApolipoproteins ECalcitriolInternal medicineHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansGenetic Predisposition to DiseaseRetinoid X Receptor alphaMacrophagesAngiotensin IIMice Inbred C57BLAortic DissectionDisease Models Animal030104 developmental biologyEndocrinologychemistryReceptors CalcitriolAortic Aneurysm AbdominalArteriosclerosis, Thrombosis, and Vascular Biology
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HIF-1α and HIF-2α Are Differentially Regulated In vivo in Neuroblastoma: High HIF-1α Correlates Negatively to Advanced Clinical Stage and Tumor Vascu…

2009

Abstract Purpose: Hypoxia is considered to be a major driving force behind tumor angiogenesis. The stabilization and activation at hypoxia of the hypoxia-inducible factors HIF-1α and HIF-2α and the concomitant induction of expression of vascular endothelial growth factor (VEGF) and other proangiogenic factors provide a molecular frame for hypoxia-driven tumor angiogenesis. This study has investigated how HIF and VEGF protein levels relate to each other with regard to vascularization, tumor stage, and overall survival in neuroblastoma. Experimental Design: Tissue cores taken from tumor specimens representing 93 children with neuroblastoma were arranged on a microarray and stained for HIF-1α,…

MaleVascular Endothelial Growth Factor ACD31Cancer ResearchPathologymedicine.medical_specialtyBiologyModels BiologicalNeovascularizationchemistry.chemical_compoundIn vivoNeoplasmsNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsmedicineHumansHypoxiaRegulation of gene expressionNeovascularization PathologicInfantCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseGene Expression Regulation NeoplasticPlatelet Endothelial Cell Adhesion Molecule-1Vascular endothelial growth factorTreatment OutcomeHIF1AOncologychemistryChild PreschoolCancer researchFemalemedicine.symptomClinical Cancer Research
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Engineered microenvironments for synergistic VEGF - Integrin signalling during vascularization

2017

We have engineered polymer-based microenvironments that promote vasculogenesis both in vitro and in vivo through synergistic integrin-growth factor receptor signalling. Poly(ethyl acrylate) (PEA) triggers spontaneous organization of fibronectin (FN) into nanonetworks which provide availability of critical binding domains. Importantly, the growth factor binding (FNIII12-14) and integrin binding (FNIII9-10) regions are simultaneously available on FN fibrils assembled on PEA. This material platform promotes synergistic integrin/VEGF signalling which is highly effective for vascularization events in vitro with low concentrations of VEGF. VEGF specifically binds to FN fibrils on PEA compared to …

MaleVascular Endothelial Growth Factor AIntegrinsBiophysicsNeovascularization PhysiologicBioengineeringpoly(ethyl acrylate)ArticleBiomaterialsHuman Umbilical Vein Endothelial CellsImage Processing Computer-AssistedAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesFibronectinTissue EngineeringPhospholipase C gammaProtein assemblyVascularizationVEGFFibronectinsMice Inbred C57BLCellular MicroenvironmentMechanics of MaterialsFocal Adhesion Protein-Tyrosine KinasesFISICA APLICADAMutationCeramics and CompositesINGENIERIA ELECTRICAGrowth factorsProtein BindingSignal Transduction
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Angiogenesis in Wounds Treated by Microdeformational Wound Therapy.

2011

BACKGROUND:: Mechanical forces play an important role in tissue neovascularization and are a constituent part of modern wound therapies. The mechanisms by which vacuum assisted closure (VAC) modulates wound angiogenesis are still largely unknown. OBJECTIVE:: To investigate how VAC treatment affects wound hypoxia and related profiles of angiogenic factors as well as to identify the anatomical characteristics of the resultant, newly formed vessels. METHODS:: Wound neovascularization was evaluated by morphometric analysis of CD31-stained wound cross-sections as well as by corrosion casting analysis. Wound hypoxia and mRNA expression of HIF-1α and associated angiogenic factors were evaluated by…

MaleVascular Endothelial Growth Factor APathologymedicine.medical_specialtyWound therapyAngiogenesismedicine.medical_treatmentNeovascularization PhysiologicOcclusive DressingsArticleNeovascularizationMiceNegative-pressure wound therapymedicineAnimalsSkinWound Healingintegumentary systemReverse Transcriptase Polymerase Chain Reactionbusiness.industryGranulation tissueBiomechanical PhenomenaMice Inbred C57BLOxygenPlatelet Endothelial Cell Adhesion Molecule-1Occlusive dressingVascular endothelial growth factor Amedicine.anatomical_structureMicrovesselsGranulation TissueCancer researchSurgerymedicine.symptombusinessWound healingNegative-Pressure Wound Therapy
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Zoledronic acid induces a significant decrease of circulating endothelial cells and circulating endothelial precursor cells in the early prostate can…

2012

<b><i>Purpose:</i></b> Published data demonstrated that zoledronic acid (ZOL) exhibits antiangiogenetic effects. A promising tool for monitoring antiangiogenic therapies is the measurement of circulating endothelial cells (CECs) and circulating endothelial precursor cells (CEPs) in the peripheral blood of patients. Our aim was to investigate the effects of ZOL on levels of CECs and CEPs in localized prostate cancer. <b><i>Methods:</i></b> Ten consecutive patients with a histologic diagnosis of low-risk prostate adenocarcinoma were enrolled and received an intravenous infusion of ZOL at baseline (T0), 28 days (T28) and 56 days (T56). Blood samp…

Malemedicine.medical_specialtyPathologyCancer ResearchBone Density Conservation AgentAngiogenesismedicine.medical_treatmentUrologyAngiogenesis InhibitorsAngiogenesis; Circulating endothelial cells; Circulating endothelial precursor cells; Prostate cancer; Zoledronic acid; Aged; Angiogenesis Inhibitors; Bone Density Conservation Agents; Cell Movement; Diphosphonates; Endothelial Cells; Humans; Imidazoles; Male; Middle Aged; Neoadjuvant Therapy; Prostatic Neoplasms; Stem Cells; Medicine (all); Oncology; Cancer ResearchFlow cytometryProstate cancerCirculating endothelial cellCell MovementStem CellPrecursor cellMedicineHumansImidazoleNeoadjuvant therapyZoledronic acidAgedEndothelial CellProstate cancermedicine.diagnostic_testBone Density Conservation AgentsDiphosphonatesbusiness.industryStem CellsMedicine (all)ImidazolesEndothelial CellsProstatic NeoplasmsGeneral MedicineMiddle Agedmedicine.diseasePeripheral bloodNeoadjuvant TherapyAngiogenesiZoledronic acidDiphosphonateOncologyCirculating endothelial precursor cellProstatic NeoplasmStem cellbusinessmedicine.drugAngiogenesis InhibitorHuman
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The involvement of MMP-2 and MMP-9 in heart exercise-related angiogenesis

2013

Background Little is known about the involvement of matrix metalloproteinases (MMPs) in cardiac vascular remodelling induced by exercise. Our aim was to evaluate and localize MMP-2 and MMP-9’s activities in relation to capillary proliferation in mouse hearts trained for 15, 30 and 45 days. Methods Sixty-three mice were randomly assigned to 7 groups: four control sedentary groups (C0, C15, C30 and C45) and three groups trained by an endurance protocol (T15, T30 and T45). MMP-2 and MMP-9 were examined with zymography and immunostaining analyses. Capillary proliferation was evaluated counting the number of CD31-positive cells. Results Different activity patterns of the latent form of both MMPs…

Malemedicine.medical_specialtyPathologyCapillary growthAngiogenesisNeovascularization PhysiologicBiologyMatrix metalloproteinaseGeneral Biochemistry Genetics and Molecular BiologyVascular remodelling in the embryoNeovascularizationMicePhysical Conditioning AnimalInternal medicineCardiac remodellingmedicineAnimalsAerobic exerciseZymographyMyocardiocyteAerobic trainingMedicine(all)Settore M-EDF/02 - Metodi E Didattiche Delle Attivita' SportiveBiochemistry Genetics and Molecular Biology(all)ResearchCapillary growthGeneral MedicineCoronary VesselsCapillariesPlatelet Endothelial Cell Adhesion Molecule-1Matrix metalloproteinasesEndocrinologyMatrix Metalloproteinase 9Capillary growth Matrix metalloproteinases Aerobic training Myocardiocyte Cardiac remodellingMatrix Metalloproteinase 2Electrophoresis Polyacrylamide Gelmedicine.symptomImmunostainingJournal of Translational Medicine
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