Search results for "Cell Movement"

showing 10 items of 396 documents

Subtypes of glial cells in the Drosophila embryonic ventral nerve cord as related to lineage and gene expression

2008

In the Drosophila embryonic CNS several subtypes of glial cells develop, which arrange themselves at characteristic positions and presumably fulfil specific functions. The mechanisms leading to the specification and differentiation of glial subtypes are largely unknown. By DiI labelling in glia-specific Gal4 lines we have clarified the lineages of the lateral glia in the embryonic ventral nerve cord and linked each glial cell to a specific stem cell. For the lineage of the longitudinal glioblast we show that it consists of 9 cells, which acquire at least four different identities. A large collection of molecular markers (many of them representing transcription factors and potential Gcm targ…

Genetic MarkersEmbryologyLineage (genetic)CellBiologyNervous SystemCell LineGlioblastCell MovementPeripheral Nervous SystemmedicineAnimalsCluster AnalysisCell LineageTranscription factorIn Situ HybridizationCell MembraneGene Expression Regulation DevelopmentalCell DifferentiationAnatomyEmbryonic stem cellCell biologyNeuroepithelial cellDrosophila melanogastermedicine.anatomical_structureGenetic Techniquesnervous systemVentral nerve cordStem cellNeurogliaDevelopmental BiologyMechanisms of Development
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Profilin1 activity in cerebellar granule neurons is required for radial migration in vivo.

2014

Neuron migration defects are an important aspect of human neuropathies. The underlying molecular mechanisms of such migration defects are largely unknown. Actin dynamics has been recognized as an important determinant of neuronal migration, and we recently found that the actin-binding protein profilin1 is relevant for radial migration of cerebellar granule neurons (CGN). As the exploited brain-specific mutants lacked profilin1 in both neurons and glial cells, it remained unknown whether profilin1 activity in CGN is relevant for CGN migration in vivo. To test this, we capitalized on a transgenic mouse line that expresses a tamoxifen-inducible Cre variant in CGN, but no other cerebellar cell …

Genetically modified mouseCerebellumNeurogenesisShort CommunicationMutantMice TransgenicBiologyCellular and Molecular NeuroscienceMiceProfilinsIn vivoCell MovementCerebellummedicineAnimalsActin-binding proteinNeuronsCell BiologyActinsCell biologyTreadmillingmedicine.anatomical_structureProfilinCerebellar cortexbiology.proteinNeurogliaCell adhesionmigration
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C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation

2015

Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa−/−) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa−/− mi…

Genetics and Molecular Biology (all)0301 basic medicinePROTEINGeneral Physics and AstronomyMELANOMAApoptosisInbred C57BLBiochemistryDISEASEAnimals; Apoptosis; Cell Line Tumor; Cell Movement; Cell Proliferation; Complement Activation; Complement C1q; Complement C3; Complement C5; Humans; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasms; Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)Micefluids and secretionsCell Movementimmune system diseasesNeoplasmsIMMUNE-RESPONSEskin and connective tissue diseasesComplement ActivationComplement C1qMice KnockoutComplement component 5TumorMultidisciplinaryQChemistry (all)Complement C5Complement C33. Good healthCell biologyMultidisciplinary SciencesDEFICIENCYmedicine.anatomical_structureScience & Technology - Other TopicsHumanKnockoutSciencechemical and pharmacologic phenomenaBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyTROPHOBLAST INVASIONMECHANISMSCell LinePhysics and Astronomy (all)03 medical and health sciencesClassical complement pathwayImmune systemINFLAMMATIONCell Line TumormedicineAnimalsHumansCell ProliferationScience & TechnologyBiochemistry Genetics and Molecular Biology (all)AnimalCell growthEFFECTOR SYSTEMComplement C1qApoptosiGeneral ChemistryComplement systemMice Inbred C57BL030104 developmental biologyCancer cellNeoplasmBone marrowANTIBODY THERAPYNature Communications
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Drp1 Controls Effective T Cell Immune-Surveillance by Regulating T Cell Migration, Proliferation, and cMyc-Dependent Metabolic Reprogramming

2018

Summary Mitochondria are key players in the regulation of T cell biology by dynamically responding to cell needs, but how these dynamics integrate in T cells is still poorly understood. We show here that the mitochondrial pro-fission protein Drp1 fosters migration and expansion of developing thymocytes both in vitro and in vivo. In addition, we find that Drp1 sustains in vitro clonal expansion and cMyc-dependent metabolic reprogramming upon activation, also regulating effector T cell numbers in vivo. Migration and extravasation defects are also exhibited in Drp1-deficient mature T cells, unveiling its crucial role in controlling both T cell recirculation in secondary lymphoid organs and acc…

Genetics and Molecular Biology (all)0301 basic medicinecell migrationT-LymphocytesCellCell CountMitochondrionLymphocyte ActivationBiochemistryCell MovementHomeostasismetabolic reprogrammingcell migration; cell proliferation; cMyc; Drp1; exhaustion; metabolic reprogramming; mitochondrial dynamics; T cells; thymocytes; tumor immune-surveillance; Biochemistry Genetics and Molecular Biology (all)lcsh:QH301-705.5cMycImmunologic SurveillanceMice KnockoutThymocytesEffectorDrp1; T cells; cMyc; cell migration; cell proliferation; exhaustion; metabolic reprogramming; mitochondrial dynamics; thymocytes; tumor immune-surveillanceCell migrationCell DifferentiationCell biologymedicine.anatomical_structurePhenotypeDynaminsendocrine systemSettore BIO/06Cell SurvivalLymphoid TissueMAP Kinase Signaling SystemT cellT cellsReceptors Antigen T-CellDrp1BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleProto-Oncogene Proteins c-myc03 medical and health sciencestumor immune-surveillancemitochondrial dynamicexhaustionHomeostasimedicineAnimalsCell ProliferationTumor microenvironmentBiochemistry Genetics and Molecular Biology (all)Cell growthAnimalT cellthymocytemitochondrial dynamicsDynamin030104 developmental biologylcsh:Biology (General)T-LymphocyteT cell migration
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A BMP7 Variant Inhibits Tumor Angiogenesis In Vitro and In Vivo through Direct Modulation of Endothelial Cell Biology

2015

Bone morphogenetic proteins (BMPs), members of the TGF-β superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Using an in vitro co-culture endothelial cord formation assay, we investigated the role of a BMP7 variant (BMP7v) in VEGF, bFGF, and tumor-driven angiogenesis. BMP7v treatment led to disruption of neo-endothelial cord formation and regression of existing VEGF and bFGF cords in vitro. Using a series of tumor cell models capable of driving angiogenesis in vitro, BMP7v treatment completely blocked cord formation. Pre-treatment of endothelial cells with BMP7v significantly reduced their cord forming ability, indicating …

Genetics and Molecular Biology (all)MaleVascular Endothelial Growth Factor AFibroblast Growth FactorAngiogenesisBone Morphogenetic Protein 7Nudelcsh:MedicineSmad ProteinsFibroblast growth factorBiochemistryNeovascularizationMiceCell Movementlcsh:ScienceBMP7 Angiogenesis TumorTumorMultidisciplinaryCell DeathNeovascularization PathologicMedicine (all)Cell migrationCell biologyEndothelial stem cellSettore MED/26 - NEUROLOGIAVascular endothelial growth factor ADrug CombinationsAdipose TissueAdipose Tissue; Animals; Bone Morphogenetic Protein 7; Cell Death; Cell Line Tumor; Cell Movement; Cell Proliferation; Collagen; Drug Combinations; Endothelial Cells; Fibroblast Growth Factor 2; Glioblastoma; Human Umbilical Vein Endothelial Cells; Humans; Laminin; Male; Mice Nude; Neoplastic Stem Cells; Neovascularization Pathologic; Neovascularization Physiologic; Proteoglycans; Receptor Fibroblast Growth Factor Type 1; Signal Transduction; Smad Proteins; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Xenograft Model Antitumor Assays; Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Neoplastic Stem CellsFibroblast Growth Factor 2ProteoglycansCollagenmedicine.symptomReceptorType 1Research ArticleSignal TransductionMice NudeNeovascularization PhysiologicBMP7BiologyCell LineSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansAgricultural and Biological Sciences (all); Biochemistry Genetics and Molecular Biology (all); Medicine (all)Receptor Fibroblast Growth Factor Type 1PhysiologicNeovascularizationCell ProliferationPathologicMatrigelBiochemistry Genetics and Molecular Biology (all)lcsh:REndothelial CellsKinase insert domain receptorVascular Endothelial Growth Factor Receptor-2Xenograft Model Antitumor AssaysAgricultural and Biological Sciences (all)lcsh:QAngiogenesisLamininGlioblastomaPLoS ONE
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Planar Cell Polarity Signaling in Collective Cell Movements During Morphogenesis and Disease

2012

Collective and directed cell movements are crucial for diverse developmental processes in the animal kingdom, but they are also involved in wound repair and disease. During these processes groups of cells are oriented within the tissue plane, which is referred to as planar cell polarity (PCP). This requires a tight regulation that is in part conducted by the PCP pathway. Although this pathway was initially characterized in flies, subsequent studies in vertebrates revealed a set of conserved core factors but also effector molecules and signal modulators, which build the fundamental PCP machinery. The PCP pathway in Drosophila regulates several developmental processes involving collective cel…

GeneticsHeart morphogenesisOmmatidial rotationConvergent extensionCollective cell movementsMorphogenesisPlanar cell polarity.BiologyDevelopmentEmbryonic stem cellDorsal closureArticleGeneticsEye developmentMorphogenesisDrosophilaDiseaseNeural crest cell migrationNeuroscienceGenetics (clinical)
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Effects of primary- and secondary-treated bleached kraft mill effluents on the immune system and physiological parameters of roach.

2000

The present study was designed to examine, whether, effluents from a modern pulp and paper mill using elemental chlorine-free/total chlorine-free (ECF/TCF) bleaching, exert effects on the immune system of fish and, in addition, to relate these findings to physiological parameters known to be affected by bleached kraft-mill effluents (BKME). Roach (Rutilus rutilus) were exposed in laboratory conditions to primary- or secondary-treated effluent from a pulp and paper mill. In order to study their capability to respond to foreign antigens they were immunised with bovine gamma-globulin (BGG) prior to exposure. The number of anti-BGG antibody-secreting cells (ASC) and the number of immunoglobulin…

GillsPaperHydrocortisoneNeutrophilsHealth Toxicology and MutagenesisIndustrial WasteSpleenEnzyme-Linked Immunosorbent AssayFresh WaterAquatic Scienceengineering.materialAndrologyImmune systemAntigenCell MovementmedicineCytochrome P-450 CYP1A1AnimalsLymphocytesRespiratory BurstAdenosine Triphosphatasesbiologybusiness.industryPulp (paper)FishesPaper millWater-Electrolyte Balancebiology.organism_classificationLiver Glycogenmedicine.anatomical_structureImmunoglobulin MImmune SystemImmunologyengineeringOsmoregulationbiology.proteinCarbohydrate MetabolismRutilusAntibodyChlorinebusinessWater Pollutants ChemicalAquatic toxicology (Amsterdam, Netherlands)
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Glycine receptors influence radial migration in the embryonic mouse neocortex.

2011

To investigate whether glycine receptors influence radial migration in the neocortex, we analyzed the effect of glycine and the glycinergic antagonist strychnine, on the distribution of 5-bromo-2'deoxyuridine-labeled neurons in organotypic slice cultures from embryonic mice cortices. Application of glycine impeded radial migration only in the presence of the glycine-transport blockers, ALX-5407 and ALX-1393. This effect was blocked by the specific glycine receptor antagonist strychnine, whereas application of strychnine in the absence of glycine was without effect. We conclude from these observations that an activation of glycine receptors can impede radial migration, but that the glycinerg…

GlycineCell CountNeocortexBiologychemistry.chemical_compoundMiceOrgan Culture TechniquesReceptors GlycineCell MovementGlial Fibrillary Acidic ProteinmedicineAnimalsDrug InteractionsReceptorGlycine receptorNeuronsNeocortexGeneral NeuroscienceAntagonistGlycine AgentsSarcosineGlycine receptor antagonistStrychnineStrychnineEmbryo MammalianCell biologymedicine.anatomical_structurechemistryBromodeoxyuridineCerebral cortexPhosphopyruvate HydrataseGlycineNeuroscienceNeuroreport
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Differential specificity of substrate-attached lectins stimulating spreading of GH3-cells under serum-free, hormone-supplemented culture conditions

1982

Most mammalian cells are capable of growth in culture only when they are supplied with an appropriate substrate to which they can adhere and spread. To prepare suitable substrates different lectins were attached onto polystyrene tissue-culture dishes after coating with polylysine. GH3-cells (a pituitary-tumor-cell line) were seeded into the culture dishes containing serum-free, hormone-supplemented medium. When succinylated Concanavalin A (s-Con A), which binds specifically to mannose residues, is attached to the surface an extraordinary spreading of GH3-cells is induced within 15 to 20 min after seeding. Other lectins with a different sugar-binding specificity are less effective in inducin…

HistologyCellMannosePituitary neoplasmBiologyCell LinePathology and Forensic MedicineStructure-Activity Relationshipchemistry.chemical_compoundCell MovementLectinsCell AdhesionConcanavalin AmedicineAnimalsPituitary NeoplasmsCell adhesionSubstrate (chemistry)Cell BiologyHormonesCulture MediaKineticsmedicine.anatomical_structurechemistryBiochemistryCell cultureConcanavalin APolylysinebiology.proteinMannoseCell and Tissue Research
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Mutant p53 gain of function can be at the root of dedifferentiation of human osteosarcoma MG63 cells into 3AB-OS cancer stem cells

2014

Osteosarcoma is a highly metastatic tumor affecting adolescents, for which there is no second-line chemotherapy. As suggested for most tumors, its capability to overgrow is probably driven by cancer stem cells (CSCs), and finding new targets to kill CSCs may be critical for improving patient survival. TP53 is the most frequently mutated tumor suppressor gene in cancers and mutant p53 protein (mutp53) can acquire gain of function (GOF) strongly contributing to malignancy. Studies thus far have not shown p53-GOF in osteosarcoma. Here, we investigated TP53 gene status/role in 3AB-OS cells-a highly aggressive CSC line previously selected from human osteosarcoma MG63 cells-to evaluate its involv…

HistologyTumor suppressor genePhysiologyEndocrinology Diabetes and MetabolismApoptosisIn situ hybridizationBiologyTNF-Related Apoptosis-Inducing LigandCell MovementCancer stem cellCell Line TumorSettore BIO/10 - BiochimicaBiomarkers TumormedicineHumansNeoplasm Invasiveness3AB-OS cells CSCs Cancer cell dedifferentiation Cancer stem cells FISH Fluorescent in situ hybridization GOF Gain of function Human osteosarcoma MMPs Matrix metalloproteinases Mutant p53 Mutant p53 gain of function Mutp53 OS OsteosarcomaClonogenic assayTumor Stem Cell AssayCell ProliferationMembrane Potential MitochondrialOsteosarcomaCancerReceptors Death DomainCell DedifferentiationCell cyclemedicine.diseaseMolecular biologyAmino Acid SubstitutionProto-Oncogene Proteins c-bcl-2Gene Knockdown TechniquesMutationNeoplastic Stem CellsCancer researchOsteosarcomaEctopic expressionTumor Suppressor Protein p53Bone
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