Search results for "Tube formation"

showing 10 items of 30 documents

Abstract A18: miR-9 and miR-200 regulate PDGFRβ-mediated endothelial differentiation of neoplastic cells in triple-negative breast cancer

2016

Abstract Tumor vascularization is a fundamental step in solid tumor progression and is orchestrated by different pathways of vasculogenesis. In malignant tumors, neoplastic cells can differentiate into endothelial-like cells acquiring the expression of endothelial markers (i.e. CD31 and CD34) and participating in the formation of vascular-like structures that functionally deliver oxygen and nutrients to the tumor site. We recently identified PDGFRβ as an important player of this process in triple negative breast cancer (TNBC). Interestingly, increasing evidence supported a connection between PDGFRβ and epithelial to mesenchymal transition (EMT), important step for the endothelial trans-diff…

Tube formationCD31Cancer ResearchMatrigelPathologymedicine.medical_specialtyCD34BiologyVasculogenesisOncologymicroRNACancer researchmedicineEpithelial–mesenchymal transitionTriple-negative breast cancerCancer Research
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Abstract 5135: Exosomes released by K562 chronic myeloid leukemia cells promote endothelial cell tubular differentiation through uptake and cell-to-c…

2011

Abstract We hypothesized that exosomes were a venue through which to transfer pro-angiogenic stimuli into and between endothelial cells during endothelial cell tubular differentiation. Exosomes are microvesicles of endocytic origin released by most normal and tumor cells that play an important role in cell-to-cell communication. Angiogenesis is recognized to be a factor in progression of chronic myeloid leukemia (CML). However, the mechanism through which this happens has not been elucidated. We first optimized and characterized secretion of exosomes from CML K562 cells, showing expected selective enrichment of exosomal markers CD63, CD81 and Tsg101 in exosomes compared to the K562 whole ce…

Tube formationCancer ResearchMatrigelAngiogenesisGrowth factormedicine.medical_treatmentBiologyExosomeMicrovesiclesCell biologyEndothelial stem cellOncologymedicineK562 cellsCancer Research
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Abstract 20: Inhibition of mutant EGFR in NSCLC promotes endothelin-1-mediated NSCLC disease progression and angiogenesis

2018

Abstract Despite recent advances in the treatment of NSCLC targeting of EGFR kinase domain mutations with tyrosine kinase inhibitors (TKIs), work needs to be done to reduce morbidity and improve survival for NSCLC patients. In NSCLC, tumor angiogenesis has been identified as important therapeutic target in combination with EGFR TKIs. However, only small advancements have been made for the use of angiogenesis inhibitors in NSCLC and it remains elusive why the inhibition of VEGF-mediated neovascularization is not therapeutically efficacious. We present evidence that a subpopulation of NSCLC cells with the EGFR TKI-induced epithelial to mesenchymal transition (EMT) contributes to the attenuati…

Tube formationCancer Researchbusiness.industryAngiogenesisCancermedicine.diseaserespiratory tract diseasesNeovascularizationGefitinibOncologymedicineCancer researchEpithelial–mesenchymal transitionmedicine.symptombusinessTyrosine kinaseEGFR inhibitorsmedicine.drugCancer Research
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Abstract 4372: Chronic myeloid leukemia (CML) exosomes promote angiogenesis in a Src-dependent fashion in vitro and in vivo

2012

Abstract CML is an uncontrolled proliferation of bone marrow myeloid cells driven by the constitutively active fusion product tyrosine kinase BCR/ABL. Angiogenesis, the formation of new blood vessels from pre-existing vasculature, is newly recognized as a factor in CML progression. Exosomes, released by a broad spectrum of cells, are microvesicles that play an important role in cell-to-cell communication both in physiological and pathological conditions. The role of exosomes released by CML cells in angiogenesis is emerging; however, little is known about the mechanisms involved in this process. We first isolated and characterized exosomes released by K562 CML cells and we demonstrated thei…

Tube formationCancer Researchmedicine.medical_specialtyAngiogenesisbusiness.industryImatinibExosomeMicrovesiclesDasatinibEndocrinologyOncologyhemic and lymphatic diseasesInternal medicineCancer researchmedicinebusinessTyrosine kinasemedicine.drugProto-oncogene tyrosine-protein kinase SrcCancer Research
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Sonic Hedgehog-Mediated Synergistic Effects Guiding Angiogenesis and Osteogenesis

2012

Sonic hedgehog (Shh) is a morphogen controlling the skeletal and vascular development in the embryo but is also reactivated during adult repair processes. Thus, this molecule holds great therapeutic potential for biotechnological and biomedical approaches aiming to enhance tissue regeneration or to replace damaged tissues. According to present knowledge, Shh signaling controls the expression of several families of growth factors involved in neovascularization and vessel maturation and acts upstream of the most prominent angiogenic growth factor, vascular endothelial growth factor. In this context, a very interesting feature of Shh is that it controls both angiogenic activity and vessel stab…

Tube formationPathologymedicine.medical_specialtyanimal structuresbiologyAngiogenesisGrowth factormedicine.medical_treatmentMural cellCell biologyEndothelial stem cellembryonic structuresbiology.proteinmedicineSonic hedgehogBone regenerationMorphogen
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2021

Tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors predominate as first-line therapy options for renal cell carcinoma. When first-line TKI therapy fails due to resistance development, an optimal second-line therapy has not yet been established. The present investigation is directed towards comparing the anti-angiogenic properties of the TKIs, sorafenib and axitinib on human endothelial cells (HUVECs) with acquired resistance towards the TKI sunitinib. HUVECs were driven to resistance by continuously exposing them to sunitinib for six weeks. They were then switched to a 24 h or further six weeks treatment with sorafenib or axitinib. HUVEC growth, as well as angiogenesis (tube…

Tube formationSorafenibbiologySunitinibAngiogenesisbusiness.industryCyclin AMedicine (miscellaneous)Cell cycleurologic and male genital diseasesfemale genital diseases and pregnancy complicationsGeneral Biochemistry Genetics and Molecular BiologyAxitinibmedicinebiology.proteinCancer researchbusinessProtein kinase Bmedicine.drugBiomedicines
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Dexamethasone Inhibits the Pro-Angiogenic Potential of Primary Human Myoblasts

2021

Tissue regeneration depends on the complex processes of angiogenesis, inflammation and wound healing. Regarding muscle tissue, glucocorticoids (GCs) inhibit pro-inflammatory signalling and angiogenesis and lead to muscle atrophy. Our hypothesis is that the synthetic GC dexamethasone (dex) impairs angiogenesis leading to muscle atrophy or inhibited muscle regeneration. Therefore, this study aims to elucidate the effect of dexamethasone on HUVECs under different conditions in mono- and co-culture with myoblasts to evaluate growth behavior and dex impact with regard to muscle atrophy and muscle regeneration. Viability assays, qPCR, immunofluorescence as well as ELISAs were performed on HUVECs,…

Vascular Endothelial Growth Factor A0301 basic medicineMuscle tissueCD31endocrine systemQH301-705.5AngiogenesisMyoblasts SkeletalNeovascularization PhysiologicInflammationdexamethasonehuman primary myoblastsArticleCatalysisInorganic Chemistry03 medical and health sciences0302 clinical medicineHuman Umbilical Vein Endothelial Cellsmedicinepolycyclic compoundsHumansMyocyteBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopyHUVECsTube formationChemistryOrganic ChemistryGeneral Medicineco-cultureVEGFCoculture TechniquesMuscle atrophyComputer Science ApplicationsCell biologyChemistry030104 developmental biologymedicine.anatomical_structureGene Expression RegulationCD31medicine.symptomWound healing030217 neurology & neurosurgeryhormones hormone substitutes and hormone antagonistsInternational Journal of Molecular Sciences
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The impact of intercellular communication for the generation of complex multicellular prevascularized tissue equivalents

2019

In reconstructive surgery the use of prevascularized soft tissue equivalents is a promising approach for wound coverage of defects after tumor resection or trauma. However, in previous studies to generate soft tissue equivalents on collagen membranes, microcapillaries were restricted to superficial areas. In this study, to understand which factors were involved in the formation of these microcapillaries, the levels of the angiogenic factors vascular endothelial growth factor (VEGF), Interleukin-8 (IL-8), and basic fibroblast growth factor (bFGF) in the supernatants of the tissue equivalents were examined at various time points and conditions. Additionally, the influence of these factors on …

Vascular Endothelial Growth Factor AMaterials science0206 medical engineeringBasic fibroblast growth factor610 MedizinBiomedical EngineeringNeovascularization PhysiologicCell Communication02 engineering and technologyBiomaterialschemistry.chemical_compoundEquivalent610 Medical sciencesmedicineHumansFibroblastCells CulturedTube formationTissue EngineeringMicrocirculationInterleukin-8Metals and AlloysEndothelial CellsSoft tissueFibroblasts021001 nanoscience & nanotechnology020601 biomedical engineeringCoculture TechniquesCell biologyVascular endothelial growth factorEndothelial stem cellmedicine.anatomical_structurechemistryCeramics and CompositesFibroblast Growth Factor 20210 nano-technologyIntracellularJournal of Biomedical Materials Research Part A
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Protein kinase C   promotes angiogenic activity of human endothelial cells via induction of vascular endothelial growth factor

2008

Aims Protein kinase C (PKC) plays an important role in the regulation of angiogenesis. However, downstream targets of PKC in endothelial cells are poorly defined. Methods and results mRNA expression of vascular endothelial growth factor (VEGF) was analysed by quantitative real-time RT-PCR in human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells. siRNA was used to knockdown PKC isoforms and VEGF. Matrigel tube formation assay was used to analyse the angiogenic activity of endothelial cells. Phorbol-12-myristate-13-acetate (PMA) enhanced the ability of HUVEC to organize into tubular networks when plated on Matrigel, a phenomenon that could be prevented by PKC inhibi…

Vascular Endothelial Growth Factor Amedicine.medical_specialtyProtein Kinase C-alphaTime FactorsPhysiologyAngiogenesismedicine.medical_treatmentBlotting WesternCarbazolesNeovascularization PhysiologicBiologyPolymerase Chain ReactionCell Linechemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansRNA MessengerRNA Small InterferingCell ShapeProtein Kinase InhibitorsCells CulturedProtein kinase CTube formationMatrigelStem CellsGrowth factorEndothelial CellsUp-RegulationCell biologyEnzyme ActivationEndothelial stem cellVascular endothelial growth factorAutocrine CommunicationVascular endothelial growth factor AReceptors Vascular Endothelial Growth FactorEndocrinologychemistryTetradecanoylphorbol AcetateAngiogenesis Inducing AgentsFibroblast Growth Factor 2RNA InterferenceCardiology and Cardiovascular MedicineCardiovascular Research
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Blocking Jak/STAT signalling using tofacitinib inhibits angiogenesis in experimental arthritis

2021

Abstract Objective During rheumatoid arthritis (RA), the angiogenic processes, occurring with pannus-formation, may be a therapeutic target. JAK/STAT-pathway may play a role and the aim of this work was to investigate the inhibiting role of a JAK-inhibitor, tofacitinib, on the angiogenic mechanisms occurring during RA. Methods After ethical approval, JAK-1, JAK-3, STAT-1, STAT-3 and VEGF expression was evaluated on RA-synovial-tissues. In vitro, endothelial cells (ECs), stimulated with 20 ng/ml of VEGF and/or 1 μM of tofacitinib, were assessed for tube formation, migration and proliferation, by Matrigel, Boyden chamber assay and ki67 gene-expression. In vivo, 32 mice received collagen (coll…

medicine.medical_specialtyAngiogenesisArthritisDiseases of the musculoskeletal systemPharmacologyPyrroleMiceRheumatoid arthritis Angiogenesis TofacitinibPiperidinePiperidinesIn vivoInternal medicineMedicineAnimalsHumansPyrrolesRheumatoid arthritisRheumatoid arthritiTube formationMatrigelEndothelial CellTofacitinibbusiness.industryAnimalSynovial MembraneEndothelial Cellsmedicine.diseaseArthritis ExperimentalRheumatologyAngiogenesiPyrimidinesPyrimidineRC925-935TofacitinibRheumatoid arthritisAngiogenesisbusinessHumanResearch Article
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