Search results for "ENDOTHELIAL CELL"

showing 10 items of 497 documents

Crosstalk between osteoblasts and endothelial cells co-cultured on a polycaprolactone-starch scaffold and the in vitro development of vascularization.

2009

The reconstruction of bone defects based on cell-seeded constructs requires a functional microvasculature that meets the metabolic demands of the engineered tissue. Therefore, strategies that augment neovascularization need to be identified. We propose an in vitro strategy consisting of the simultaneous culture of osteoblasts and endothelial cells on a starch-based scaffold for the formation of pre-vascular structures, with the final aim of accelerating the establishment of a vascular bed in the implanted construct. Human dermal microvascular endothelial cells (HDMECs) were co-cultured with human osteoblasts (hOBs) on a 3D starch-based scaffold and after 21 days of culture HDMEC aligned and…

MaleVascular Endothelial Growth Factor ACell typeScaffoldMaterials sciencePolyestersBiophysicsConnexinNeovascularization PhysiologicBioengineering02 engineering and technologyBiomaterialsNeovascularizationDiffusion03 medical and health sciencesType IV collagenTissue engineeringOsteogenesismedicineHumansTissue engineeringBonePolymer030304 developmental biology0303 health sciencesScience & TechnologyOsteoblastsTissue ScaffoldsVascularizationEndothelial CellsStarch021001 nanoscience & nanotechnologyImmunohistochemistryCoculture TechniquesCell biologyCrosstalk (biology)Mechanics of MaterialsCeramics and Compositesmedicine.symptomCo-culture0210 nano-technologyType I collagenBiomedical engineeringBiomaterials
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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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Endothelial Dysfunction in Tristetraprolin-deficient Mice Is Not Caused by Enhanced Tumor Necrosis Factor-α Expression

2014

Cardiovascular events are important co-morbidities in patients with chronic inflammatory diseases like rheumatoid arthritis. Tristetraprolin (TTP) regulates pro-inflammatory processes through mRNA destabilization and therefore TTP-deficient mice (TTP(-/-) mice) develop a chronic inflammation resembling human rheumatoid arthritis. We used this mouse model to evaluate molecular signaling pathways contributing to the enhanced atherosclerotic risk in chronic inflammatory diseases. In the aorta of TTP(-/-) mice we observed elevated mRNA expression of known TTP targets like tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein-1α, as well as of other pro-atherosclerotic mediators, l…

MaleVasculitismedicine.medical_specialtyMRNA destabilizationRNA StabilityTristetraprolinInflammationBiochemistryNitric oxideMicechemistry.chemical_compoundOrgan Culture TechniquesTristetraprolinhemic and lymphatic diseasesInternal medicinemedicineAnimalsEndothelial dysfunctionMolecular BiologyAortaReactive nitrogen speciesMice KnockoutMembrane GlycoproteinsNADPH oxidasebiologyTumor Necrosis Factor-alphaEndothelial CellsNADPH OxidasesMolecular Bases of DiseaseCell Biologyrespiratory systemAtherosclerosismedicine.diseaseReactive Nitrogen SpeciesMice Inbred C57BLOxidative StressCholesterolEndocrinologychemistryMice Inbred DBAChronic DiseaseNADPH Oxidase 2biology.proteinFemaleTumor necrosis factor alphamedicine.symptomReactive Oxygen SpeciesJournal of Biological Chemistry
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Complex I dysfunction and tolerance to nitroglycerin: an approach based on mitochondrial-targeted antioxidants.

2006

Nitroglycerin (GTN) tolerance was induced in vivo (rats) and in vitro (rat and human vessels). Electrochemical detection revealed that the incubation dose of GTN (5×10 −6 mol/L) did not release NO or modify O 2 consumption when administered acutely. However, development of tolerance produced a decrease in both mitochondrial O 2 consumption and the K m for O 2 in animal and human vessels and endothelial cells in a noncompetitive action. GTN tolerance has been associated with impairment of GTN biotransformation through inhibition of aldehyde dehydrogenase (ALDH)-2, and with uncoupling of mitochondrial respiration. Feeding rats with mitochondrial-targeted antioxidants (mitoquinone [MQ]) and i…

MaleantioxidantAntioxidantPhysiologyUbiquinonemedicine.medical_treatmentMuscle RelaxationVasodilator AgentsAldehyde dehydrogenasePharmacologyMitochondrionmedicine.disease_causeAntioxidantsMuscle Smooth VascularRats Sprague-Dawleychemistry.chemical_compoundNitroglycerinDrug toleranceoxidative stressCyclic GMPchemistry.chemical_classificationbiologyAldehyde Dehydrogenase MitochondrialDrug ToleranceGlutathioneMitochondriamitochondriaBiochemistrycardiovascular systemCardiology and Cardiovascular Medicinecirculatory and respiratory physiologyMuscle ContractionendotheliumIn Vitro TechniquesMitochondrial ProteinsOrganophosphorus CompoundsOxygen ConsumptionRespirationmedicineAnimalsHumansReactive oxygen speciesElectron Transport Complex IDose-Response Relationship DrugEndothelial CellsGlutathioneAldehyde DehydrogenasenitroglycerinRatsOxidative Stresschemistrybiology.proteinReactive Oxygen SpeciesOxidative stressCirculation research
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Aerobic training and angiogenesis activation in patients with stable chronic heart failure: a preliminary report.

2013

The pathophysiology of chronic heart failure (CHF) involves multiple hystologic and molecular alterations. To determine the effects of physical training on circulating endothelial progenitor cells (EPCs), angiogenesis (angiogenin, angiopoietin-1 and -2, VEGF, Tie-2, SDF-1α) and inflammation (IL-6, CRP), we compared data obtained from 11 CHF pts before and after 3 months aerobic exercise training, to those from 10 non trained CHF pts (CHF-C group, age 64 + 2 years, NYHA 2). At the end of the study, EPCs count and AP-2 serum levels significantly increased in the CHF-TR group. These preliminary data suggest a significant effect of even a short program of physical training on angiogenic activat…

Malemedicine.medical_specialtyAngiogeninBrachial ArteryAngiogenesisHealth Toxicology and MutagenesisClinical BiochemistryNeovascularization PhysiologicCardiovascular disease growth factors/cytokines/inflammatory mediators sports science/exerciseInflammationPilot ProjectsBiochemistryNeovascularizationInternal medicinemedicineAerobic exerciseHumanscardiovascular diseasesProspective StudiesEndothelial dysfunctionAngiogenic ProteinsExerciseAgedHeart Failurebusiness.industryStem CellsEndothelial CellsStroke VolumeStroke volumeMiddle Agedmedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareExercise TherapyVasodilationTreatment OutcomeHeart failureImmunologyChronic Diseasecardiovascular systemCardiologymedicine.symptombusinessBiomarkerscirculatory and respiratory physiologyBiomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals
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CXCR2 blockade impairs angiotensin II-induced CC chemokine synthesis and mononuclear leukocyte infiltration.

2007

Objective—Angiotensin II (Ang-II) and mononuclear leukocytes are involved in atherosclerosis. This study reports the inhibition of Ang-II–induced mononuclear cell recruitment by CXCR2 antagonism and the mechanisms involved.Methods and Results—Ang-II (1 nmol/L, i.p. in rats) induced CXC and CC chemokines, followed by neutrophil and mononuclear cell recruitment. Administration of the CXCR2 antagonist, SB-517785-M, inhibited the infiltration of both neutrophils (98%) and mononuclear cells (60%). SB-517785-M had no effect on the increase in CXC chemokine levels but reduced MCP-1, RANTES, and MIP-1α release by 66%, 63%, and 80%, respectively. Intravital microscopy showed that pretreatment with S…

Malemedicine.medical_specialtyChemokineCXCR3Peripheral blood mononuclear cellLosartanReceptors Interleukin-8BRats Sprague-DawleyChemokine receptorInternal medicinemedicineCell AdhesionCCL17AnimalsHumansCXC chemokine receptorsSplanchnic CirculationChemokine CCL7Chemokine CCL4Chemokine CCL5Cells CulturedChemokine CCL2Chemokine CCL3InflammationbiologyAngiotensin IIMicrocirculationEndothelial CellsMacrophage Inflammatory ProteinsAtherosclerosisAngiotensin IIMonocyte Chemoattractant ProteinsRatsMononuclear cell infiltrationChemotaxis LeukocyteEndocrinologyNeutrophil Infiltrationbiology.proteinLeukocytes MononuclearCardiology and Cardiovascular MedicineAngiotensin II Type 1 Receptor BlockersArteriosclerosis, thrombosis, and vascular biology
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Estradiol selectively stimulates endothelial prostacyclin production through estrogen receptor-α

2010

Estradiol (E2) acts on the endothelium to promote vasodilatation through the release of several compounds, including prostanoids, which are products of arachidonic acid metabolism. Among these, prostacyclin (PGI2) and thromboxane A2 (TXA2) exert opposite effects on vascular tone. The role of different estrogen receptors (ERs) in the PGI2/TXA2 balance, however, has not been fully elucidated. Our study sought to uncover whether E2 enhances basal production of PGI2 or TXA2 in cultured human umbilical vein endothelial cells (HUVECs), to analyze the enzymatic mechanisms involved, and to evaluate the different roles of both types of ERs (ERα and ERβ). HUVECs were exposed to E2, selective ERα (1,3…

Malemedicine.medical_specialtyEndotheliumDiarylpropionitrileEstrogen receptorProstacyclinBiologyThromboxane A2chemistry.chemical_compoundThromboxane A2EndocrinologyCytochrome P-450 Enzyme SystemInternal medicinemedicineEstrogen Receptor betaHumansMolecular BiologyCells CulturedEstradiolGroup IV Phospholipases A2Estrogen Receptor alphaEndothelial CellsProstanoidEpoprostenolIntramolecular OxidoreductasesEndocrinologymedicine.anatomical_structurechemistryCyclooxygenase 1cardiovascular systembiology.proteinFemalelipids (amino acids peptides and proteins)Endothelium VascularThromboxane-A synthaseEstrogen receptor alphamedicine.drugJournal of Molecular Endocrinology
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Impaired Vitamin D Signaling in Endothelial Cell Leads to an Enhanced Leukocyte-Endothelium Interplay: Implications for Atherosclerosis Development

2015

Endothelial cell activation leading to leukocyte recruitment and adhesion plays an essential role in the initiation and progression of atherosclerosis. Vitamin D has cardioprotective actions, while its deficiency is a risk factor for the progression of cardiovascular damage. Our aim was to assess the role of basal levels of vitamin D receptor (VDR) on the early leukocyte recruitment and related endothelial cell-adhesion-molecule expression, as essential prerequisites for the onset of atherosclerosis. Knockdown of VDR in endothelial cells (shVDR) led to endothelial cell activation, characterized by upregulation of VCAM-1, ICAM-1 and IL-6, decreased peripheral blood mononuclear cell (PBMC) ro…

Malemedicine.medical_specialtyEndotheliumMedicinalcsh:MedicineDown-RegulationVascular Cell Adhesion Molecule-1InflammationCell CommunicationBiologyCalcitriol receptorCell LineEndothelial activationMiceEndothelial cellNF-KappaB Inhibitor alphaInternal medicineCell AdhesionmedicineAnimalsHumansMacrophageEndotheliumVitamin Dlcsh:ScienceCell adhesionMultidisciplinaryInterleukin-6lcsh:RNF-kappa BEndothelial CellsAtherosclerosisIntercellular Adhesion Molecule-1Plaque AtheroscleroticUp-RegulationMice Inbred C57BLEndothelial stem cellIκBαmedicine.anatomical_structureEndocrinologyLeukocytes MononuclearReceptors Calcitriollcsh:QFemaleI-kappa B Proteinslipids (amino acids peptides and proteins)medicine.symptomSignal TransductionResearch ArticlePLOS ONE
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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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