Search results for " molecule"

showing 10 items of 1523 documents

Role of S128R polymorphism of E-selectin in colon metastasis formation.

2007

The extravasation of cancer cells is a key step of the metastatic cascade. Polymorphisms in genes encoding adhesion molecules can facilitate metastasis by increasing the strength of interaction between tumor and endothelial cells as well as impacting other properties of cancer cells. We investigated the Ser128Arg (a561c at the nucleotide level) polymorphism in the E-selectin gene in patients with metastatic colon cancer and its functional significance. Genotyping for a561c polymorphism was performed on 172 cancer patients and on an age-matched control population. The colon cancer group was divided into groups with (M+) and without observable metastasis (M−). For in vitro functional assays, …

MaleCancer ResearchColorectal cancerBiologyArginineTransfectionMetastasise-SELECTIN; COLON CANCER METASTASISSettore BIO/13 - Biologia ApplicataCell MovementE-selectinmedicineCell AdhesionSerineTumor Cells CulturedHumansNeoplasm MetastasisPolymorphism GeneticCell adhesion moleculeCancerTransfectionMiddle Agedmedicine.diseaseExtravasationColon Carcinoma E-Selectin Metastasis PolymorphismPhenotypeOncologyImmunologyCancer cellColonic NeoplasmsCancer researchbiology.proteinFemaleE-SelectinSignal TransductionInternational journal of cancer
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Oncogene-driven intrinsic inflammation induces leukocyte production of tumor necrosis factor that critically contributes to mammary carcinogenesis.

2010

Abstract Oncogene activation promotes an intrinsic inflammatory pathway that is crucial for cancer development. Here, we have investigated the actual effect of the inflammatory cytokine tumor necrosis factor (TNF) on the natural history of spontaneous mammary cancer in the HER2/neuT (NeuT) transgenic mouse model. Bone marrow transplantation from TNF knockout mice into NeuT recipients significantly impaired tumor growth, indicating that the source of TNF fostering tumor development was of bone marrow origin. We show that the absence of leukocyte-derived TNF disarranged the tumor vasculature, which lacked pericyte coverage and structural integrity, leading to diffuse vascular hemorrhage and s…

MaleCancer ResearchStromal cellmedicine.medical_treatmentInflammationmedicine.disease_causeAntibodiesArticleMicemedicineLeukocytesAnimalsHumansReceptors Tumor Necrosis Factor Type IItumor necrosis factor mammary carcinogenesis.Crosses GeneticBone Marrow TransplantationInflammationMice KnockoutOncogenebusiness.industryTumor Necrosis Factor-alphaCancerMammary Neoplasms ExperimentalOncogenesmedicine.diseaseImmunohistochemistryMice Inbred C57BLPlatelet Endothelial Cell Adhesion Molecule-1medicine.anatomical_structureCytokineOncologyReceptors Tumor Necrosis Factor Type IImmunologyTumor necrosis factor alphaFemaleBone marrowmedicine.symptomCarcinogenesisbusinessCancer research
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Aberrant arrested in maturation neuromuscular junctions in centronuclear myopathy

1994

Unusual ultrastructural changes of the nerve terminals have been found in an infant born with severe, fatal XLR form of centronuclear myopathy. Aberrant neuromuscular junctions in myotubes decorated by N-CAM were observed. The junction changes were manifested by simplification of postsynaptic membrane and paucity of secondary synaptic clefts. These resembles fetal neuromuscular junctions. The findings suggest that the expression of N-CAM by arrested myotubes may be promoted by abnormal nerve-muscle cell interactions, induced by motor endplate immaturity.

MaleCell Adhesion Molecules NeuronalCellNeuromuscular JunctionElectromyographyBiologyMicrotubulesMotor EndplateNeuromuscular junctionMotor EndplateMicrotubulemedicineHumansCentronuclear myopathyMotor NeuronsFetusTissue Embeddingmedicine.diagnostic_testElectromyographyMyogenesisMusclesInfantNeuromuscular Diseasesmedicine.diseaseCell biologyMicroscopy Electronmedicine.anatomical_structureNeurologySynapsesNeurology (clinical)NeuroscienceJournal of the Neurological Sciences
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Early life stress stimulates hippocampal reelin gene expression in a sex-specific manner: Evidence for corticosterone-mediated action

2010

Early life stress predisposes to the development of psychiatric disorders. In this context the hippocampal formation is of particular interest, because it is affected by stress on the structural and cognitive level. Since little is known how early life stress is translated on the molecular level, we mimicked early life stress in mouse models and analyzed the expression of the glycoprotein Reelin, a master molecule for development and differentiation of the hippocampus. From postnatal day 1 (P1) to P14, mouse pups were subjected to one of the following treatments: nonhandling (NH), handling (H), maternal separation (MS), and early deprivation (ED) followed by immediate (P15) or delayed (P70)…

MaleCell Adhesion Molecules NeuronalCognitive NeuroscienceGene ExpressionCell CountNerve Tissue ProteinsContext (language use)Hippocampal formationHippocampusMiceCajal–Retzius cellchemistry.chemical_compoundSex FactorsCorticosteronemedicineAnimalsRNA MessengerReelinBrain-derived neurotrophic factorExtracellular Matrix ProteinsMaternal deprivationbiologyMaternal DeprivationSerine EndopeptidasesDAB1Reelin Proteinmedicine.anatomical_structurenervous systemchemistrybiology.proteinFemaleCorticosteroneNeuroscienceStress PsychologicalHippocampus
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A population of prenatally generated cells in the rat paleocortex maintains an immature neuronal phenotype into adulthood.

2008

New neurons in the adult brain transiently express molecules related to neuronal development, such as the polysialylated form of neural cell adhesion molecule, or doublecortin (DCX). These molecules are also expressed by a cell population in the rat paleocortex layer II, whose origin, phenotype, and function are not clearly understood. We have classified most of these cells as a new cell type termed tangled cell. Some cells with the morphology of semilunar-pyramidal transitional neurons were also found among this population, as well as some scarce cells resembling semilunar, pyramidal. and fusiform neurons. We have found that none of these cells in layer II express markers of glial cells, m…

MaleCell typeDoublecortin ProteinAntimetabolitesCognitive NeuroscienceNeurogenesisPopulationMice Inbred StrainsNeural Cell Adhesion Molecule L1Receptors N-Methyl-D-AspartateImmunophenotypingRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundMiceReceptors GlucocorticoidPregnancyAnimalsEntorhinal CortexCyclic adenosine monophosphateeducationeducation.field_of_studyArc (protein)biologyPyramidal CellsStem CellsNeurogenesisAge FactorsPhenotypeDoublecortinCell biologyRatsMicroscopy ElectronchemistryBromodeoxyuridinebiology.proteinSialic AcidsNeural cell adhesion moleculeFemaleNeuroscienceNeurogliaBiomarkersCerebral cortex (New York, N.Y. : 1991)
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Differentiation driven by granulocyte-macrophage colony-stimulating factor endows microglia with interferon-γ-independent antigen presentation functi…

1993

The antigen presentation function of microglial cells was analyzed after differentiation in neonatal mouse brain cell cultures supplemented either with macrophage (M) or granulocyte/macrophage (GM) colony-stimulating factor (CSF). The cells separated from concomitant astrocytes in both culture systems turned out to exhibit cytological characteristics of macrophages and bore MAC-1 and F4/80 markers in a similar way. When comparatively tested for accessory cell function, only microglia developed with GM-CSF were able to efficiently induce antigen-directed proliferation of a series of helper T cell lines representing both the TH1 and TH2 subtype. Antigenic T cell activation by this microglia p…

MaleCellular differentiationT cellImmunologyAntigen presentationAntigen-Presenting CellsBiologyInterferon-gammaMiceAntigenmedicineAnimalsImmunology and AllergyMacrophageAntigen-presenting cellCells CulturedMice Inbred BALB CMicrogliaHistocompatibility Antigens Class IIBrainGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationT-Lymphocytes Helper-InducerIntercellular Adhesion Molecule-1Cell biologyGranulocyte macrophage colony-stimulating factormedicine.anatomical_structureNeurologyImmunologyFemaleNeurology (clinical)Cell Adhesion MoleculesNeurogliamedicine.drugJournal of Neuroimmunology
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Aspartoacylase-lacZ knockin mice: an engineered model of Canavan disease.

2011

Canavan Disease (CD) is a recessive leukodystrophy caused by loss of function mutations in the gene encoding aspartoacylase (ASPA), an oligodendrocyte-enriched enzyme that hydrolyses N-acetylaspartate (NAA) to acetate and aspartate. The neurological phenotypes of different rodent models of CD vary considerably. Here we report on a novel targeted aspa mouse mutant expressing the bacterial β-Galactosidase (lacZ) gene under the control of the aspa regulatory elements. X-Gal staining in known ASPA expression domains confirms the integrity of the modified locus in heterozygous aspa lacZ-knockin (aspa(lacZ/+)) mice. In addition, abundant ASPA expression was detected in Schwann cells. Homozygous (…

MaleCentral Nervous SystemCerebellumPathologyAnatomy and PhysiologyCanavan DiseaseMouseMutantlcsh:MedicineNeural HomeostasisBiochemistryMiceNeurobiology of Disease and Regenerationlcsh:ScienceSex CharacteristicsMultidisciplinaryNeuromodulationNeurochemistryGenomicsAnimal ModelsFunctional Genomicsmedicine.anatomical_structureLac OperonNeurologyHomeostatic MechanismsMedicineFemaleNeurochemicalsGenetic EngineeringResearch ArticleNervous System PhysiologyBiotechnologymedicine.medical_specialtyTransgeneCentral nervous systemNeurophysiologyMice TransgenicNeuroimagingBiologyNeurological SystemAmidohydrolasesWhite matterModel OrganismsGeneticsmedicineAnimalsBiologyNeuropeptidesLeukodystrophylcsh:RComputational Biologymedicine.diseaseMolecular biologyCanavan diseaseAspartoacylaseDisease Models AnimalMetabolismnervous systemSmall MoleculesCellular NeuroscienceMetabolic DisordersMutationGenetics of DiseaseNervous System Componentslcsh:QGene FunctionMolecular NeuroscienceAnimal GeneticsNeurosciencePLoS ONE
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Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

2011

Background Osteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint. Methodology/Principal Findings OA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was…

MaleChemokineAnatomy and PhysiologyInterleukin-1betalcsh:MedicineGene ExpressionMatrix metalloproteinaseBiochemistryCell MovementDrug Discoverylcsh:ScienceMusculoskeletal SystemCells CulturedChemokine CCL2MultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionSynovial MembraneNF-kappa BInterleukinCell migrationmedicine.anatomical_structureMedicineFemaleMatrix Metalloproteinase 3Inflammation MediatorsMatrix Metalloproteinase 1Mitogen-Activated Protein KinasesResearch ArticleCell PhysiologyBlotting WesternRheumatologySynovitisOsteoarthritisOrganometallic CompoundsmedicineHumansInterleukin 8BiologyAgedCell ProliferationChemokine CCL20lcsh:RInterleukin-8medicine.diseaseTranscription Factor AP-1CCL20Oxidative StressSmall MoleculesImmunologyCancer researchbiology.proteinlcsh:QSynovial membraneHeme Oxygenase-1PLoS ONE
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Trans- but not cis-resveratrol impairs angiotensin-II-mediated vascular inflammation through inhibition of NF-κB activation and peroxisome proliferat…

2010

Abstract Angiotensin II (Ang-II) displays inflammatory activity and is implicated in several cardiovascular disorders. This study evaluates the effect of cis- and trans (t)-resveratrol (RESV) in two in vivo models of vascular inflammation and identifies the cardioprotective mechanisms that underlie them. In vivo, Ang-II–induced arteriolar leukocyte adhesion was inhibited by 71% by t-RESV (2.1 mg/kg, i.v.), but was not affected by cis-RESV. Because estrogens influence the rennin-angiotensin system, chronic treatment with t-RESV (15 mg/kg/day, orally) inhibited ovariectomy-induced arteriolar leukocyte adhesion by 81%, partly through a reduction of cell adhesion molecule (CAM) expression and c…

MaleChemokineEndotheliumOvariectomyImmunologyInflammationAngiogenesis InhibitorsCell CommunicationPharmacologyRats Sprague-DawleyDownregulation and upregulationStilbenesmedicineImmunology and AllergyAnimalsHumansCells CulturedbiologyCell adhesion moleculeMonocyteAngiotensin IINF-kappa BStereoisomerismAngiotensin IIRatsUp-RegulationPPAR gammaDisease Models Animalmedicine.anatomical_structureCardiovascular DiseasesResveratrolImmunologybiology.proteinFemaleEndothelium Vascularmedicine.symptomSignal transductionInflammation MediatorsJournal of immunology (Baltimore, Md. : 1950)
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Bacteria-Derived Compatible Solutes Ectoine and 5α-Hydroxyectoine Act as Intestinal Barrier Stabilizers to Ameliorate Experimental Inflammatory Bowel…

2015

Earlier studies showed that the compatible solute ectoine (1) given prophylactically before induction of colitis by 2,4,6-trinitrobenzenesulfonic acid (TNBS) in rats prevented histological changes induced in the colon and the associated rise in inflammatory mediators. This study was therefore conducted to investigate whether ectoine (1) and its 5α-hydroxy derivative (2) would also be effective in treating an already established condition. Two days after inducing colitis in rats by instilling TNBS/alcohol in the colon, animals were treated orally once daily for 1 week with either 1 or 2 (50, 100, 300 mg/kg). Twenty-four hours after the last drug administration rats were sacrificed. Ulcerativ…

MaleColonInterleukin-1betaPharmaceutical SciencePharmacologyEctoineInflammatory bowel diseaseAnalytical Chemistrychemistry.chemical_compoundDrug DiscoverymedicineAnimalsHumansRats WistarColitisPeroxidasePharmacologyBacteriaMolecular StructurebiologyTumor Necrosis Factor-alphaChemistryOrganic ChemistryAmino Acids DiaminoGlutathioneColitisInflammatory Bowel DiseasesIntercellular Adhesion Molecule-1medicine.diseasebiology.organism_classificationGlutathioneRatsIntestinesSolutionsTrinitrobenzenesulfonic AcidComplementary and alternative medicineBiochemistryMyeloperoxidasebiology.proteinMolecular MedicineEgyptOsmoprotectantTumor necrosis factor alphaBacteriaJournal of Natural Products
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