Search results for "Mice"

showing 10 items of 6027 documents

ShRNA-mediated knock-down of CXCL8 inhibits tumor growth in colorectal liver metastasis.

2018

CXCL8 belongs to proinflammatory chemokines that are predominantly involved in neutrophil chemotaxis and degranulation. Several studies have suggested that secretion of CXCL8 from cancer cells have a profound effect on tumor microenvironment. In this study, in continuation to our previous work of understanding the global picture of invasion related genes in colorectal liver metastases, we clearly show an up-regulation of CXCL8 expression in the tumor cells at the invasion front as compared to the tumor cells in the inner parts of the tumor. Furthermore, ShRNA mediated down-regulation of CXCL8 resulted in inhibition of cell proliferation, viability and invasion in vitro and a near complete g…

musculoskeletal diseases0301 basic medicineAngiogenesisCell SurvivalBiophysicsDown-RegulationApoptosisBiologyBiochemistryProinflammatory cytokineMetastasis03 medical and health sciencesMice0302 clinical medicineCell Line TumormedicineAnimalsHumansNeoplasm InvasivenessAmino Acid SequenceRNA MessengerRNA Small InterferingMolecular BiologyProtein kinase BConserved SequenceCell ProliferationTumor microenvironmentInterleukin-8Liver NeoplasmsCell Biologymedicine.diseaseXenograft Model Antitumor AssaysUp-RegulationGene Expression Regulation NeoplasticVascular endothelial growth factor A030104 developmental biologyTumor progression030220 oncology & carcinogenesisGene Knockdown TechniquesCancer cellCancer researchColorectal NeoplasmsBiochemical and biophysical research communications
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Progestogens and risk of breast cancer: a link between bone and breast?

2015

This article reviews the data supporting the role of receptor activator of the nuclear factor kappa (RANK) and its ligand, RANKL, in progestogen-induced breast cancer. Both experimental and clinical studies have been included. The expression of both RANK and RANKL has been described in epithelial cells of both mice and humans. Experiments of gain and loss of function in mice have shown that RANK/RANKL mediate alveologenesis during pregnancy or the estrous cycle. Moreover, the participation of the RANK/RANKL has been detected in models of breast carcinogenesis associated with progestogens-like medroxyprogesterone acetate. Recent clinical studies have found that the expression of RANK is asso…

musculoskeletal diseases0301 basic medicineEndocrinology Diabetes and MetabolismOsteoclastsBone NeoplasmsBreast NeoplasmsMice03 medical and health sciences0302 clinical medicineEndocrinologyBreast cancerRisk FactorsmedicineAnimalsHumansMedroxyprogesterone acetateBreastReceptorProgesteroneLoss functionEstrous cyclePregnancyReceptor Activator of Nuclear Factor-kappa BbiologyActivator (genetics)business.industryRANK LigandObstetrics and Gynecologymedicine.disease030104 developmental biologyRANKL030220 oncology & carcinogenesisImmunologybiology.proteinCancer researchFemaleProgestinsbusinessmedicine.drugGynecological Endocrinology
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Mouse CSB protein is important for gene expression in the presence of a single-strand break in the non-transcribed DNA strand.

2010

CSB protein is required for strand-specific repair of bulky DNA lesions in transcribed genes and mediates transcription recovery after exposure to DNA-damaging agents. We enzymatically generated DNA single-strand breaks (SSBs) with 3'-OH and 5'-phosphate termini in defined positions of a plasmid-borne gene and measured their effect on transcription in cell lines with different statuses of the Csb gene. A single SSB in the transcribed region of the gene caused significant decrease of gene expression. In all tested cell lines of mouse and human origin, a SSB in the transcribed DNA strand was less harmful for gene expression than a SSB situated in the opposing DNA strand. CSB deficiency exhibi…

musculoskeletal diseasesBase SequenceDNA damageDNA Single-StrandedGene ExpressionCell BiologyBiologyBiochemistryMolecular biologychemistry.chemical_compoundMiceDNA Repair EnzymeschemistryTranscription (biology)Cell cultureCoding strandGene expressionAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneDNATranscription bubbleDNA DamageDNA PrimersDNA repair
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Sense and Antisense DMPK RNA Foci Accumulate in DM1 Tissues during Development.

2015

International audience; Myotonic dystrophy type 1 (DM1) is caused by an unstable expanded CTG repeat located within the DMPK gene 3'UTR. The nature, severity and age at onset of DM1 symptoms are very variable in patients. Different forms of the disease are described, among which the congenital form (CDM) is the most severe. Molecular mechanisms of DM1 are well characterized for the adult form and involve accumulation of mutant DMPK RNA forming foci in the nucleus. These RNA foci sequester proteins from the MBNL family and deregulate CELF proteins. These proteins are involved in many cellular mechanisms such as alternative splicing, transcriptional, translational and post-translational regul…

musculoskeletal diseasesCCAAT-Enhancer-Binding Protein-deltacongenital hereditary and neonatal diseases and abnormalities[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologylcsh:MedicineMice Transgenic[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMyotonin-Protein KinaseMice[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsHumansMyotonic DystrophyRNA AntisenseRNA Messengerlcsh:ScienceMuscle SkeletalCell NucleusMyocardiumlcsh:R[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyBrainGene Expression Regulation DevelopmentalRNA-Binding Proteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyEmbryo MammalianAlternative SplicingDisease Models Animal[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAnimals Newborn[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]lcsh:QTrinucleotide Repeat ExpansionSignal TransductionResearch ArticlePloS one
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Silicate modulates the cross-talk between osteoblasts (SaOS-2) and osteoclasts (RAW 264.7 cells): inhibition of osteoclast growth and differentiation

2012

It has been shown that inorganic monomeric and polymeric silica/silicate, in the presence of the biomineralization cocktail, increases the expression of osteoprotegerin (OPG) in osteogenic SaOS-2 sarcoma cells in vitro. In contrast, silicate does not affect the steady-state gene expression level of the osteoclastogenic ligand receptor activator of NF-κB ligand (RANKL). In turn it can be expected that the concentration ratio of the mediators OPG/RANKL increases in the presence of silicate. In addition, silicate enhances the growth potential of SaOS-2 cells in vitro, while it causes no effect on RAW 264.7 cells within a concentration range of 10-100 µM. Applying a co-cultivation assay system,…

musculoskeletal diseasesCell SurvivalCellular differentiationmedicine.medical_treatmentAcid PhosphataseMineralogyOsteoclastsCell Count02 engineering and technologyCell CommunicationBiochemistryCell Line03 medical and health sciencesMiceOsteoprotegerinOsteoclastOsteogenesismedicineAnimalsHumansMolecular BiologyRAW 264.7 Cells030304 developmental biologyTartrate-resistant acid phosphataseCell Proliferation0303 health sciencesOsteoblastsbiologyBone Density Conservation AgentsChemistryTartrate-Resistant Acid PhosphataseMacrophagesSilicatesRANK LigandCell DifferentiationCell Biology021001 nanoscience & nanotechnologyCoculture TechniquesCell biologyIsoenzymesmedicine.anatomical_structureCytokineCell cultureRANKLbiology.protein0210 nano-technologyJ. Cell. Biochem.
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Gastric emptying, small intestinal transit and fecal output in dystrophic (mdx) mice.

2009

Duchenne muscular dystrophy (DMD), which results from deficiency in dystrophin, a sarcolemma protein of skeletal, cardiac and smooth muscle, is characterized by progressive striated muscle degeneration, but various gastrointestinal clinical manifestations have been observed. The aim was to evaluate the possible impact of the dystrophin loss on the gastrointestinal propulsion in mdx mice (animal model for DMD). The gastric emptying of a carboxymethyl cellulose/phenol red dye non-nutrient meal was not significantly different at 20 min from gavaging between wild-type and mdx mice. The intestinal transit and the fecal output were significantly decreased in mdx versus normal animals, although th…

musculoskeletal diseasesCell physiologyDuchenne muscular dystrophyMalecongenital hereditary and neonatal diseases and abnormalitiesmdx mousemedicine.medical_specialtyPhysiologyDuchenne muscular dystrophySettore BIO/09 - FisiologiaMiceIn vivoInternal medicineIntestine SmallMedicineAnimalsmdx mouseMuscular dystrophyDefecationSarcolemmabiologyGastric emptyingbusiness.industryMuscular Dystrophy Animalmusculoskeletal systemmedicine.diseaseMice Inbred C57BLDisease Models AnimalEndocrinologyGastric Emptyingbiology.proteinFecal outputMice Inbred mdxIntestinal transitbusinessDystrophinGastrointestinal MotilityThe journal of physiological sciences : JPS
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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Targeting of the transcription factor STAT4 by antisense phosphorothioate oligonucleotides suppresses collagen-induced arthritis

2007

Abstract The transcription factor STAT4 mediates signals of various proinflammatory cytokines, such as IL-12, IL-15, and IL-23, that initiate and stabilize Th1 cytokine production. Although Th1 cytokine production has been suggested to play a major pathogenic role in rheumatoid arthritis, the role of STAT4 in this disease is poorly understood. In this study, we demonstrate a key functional role of STAT4 in murine collagen-induced arthritis (CIA). In initial studies we found that STAT4 expression is strongly induced in CD4+ T cells and to a lesser extent in CD11b+ APCs during CIA. To analyze the role of STAT4 for arthritis manifestation, we next investigated the outcome of interfering with S…

musculoskeletal diseasesImmunologyAntigen-Presenting CellsCodon InitiatorArthritisBiologyProinflammatory cytokineArthritis RheumatoidPathogenesisMiceimmune system diseasesmedicineAnimalsImmunology and Allergyskin and connective tissue diseasesSTAT4Cells CulturedMice KnockoutMice Inbred BALB CCD11b Antigenhemic and immune systemsOligonucleotides AntisenseSTAT4 Transcription FactorTh1 CellsThionucleotidesmedicine.diseaseArthritis ExperimentalIntegrin alpha MRheumatoid arthritisImmunologybiology.proteinExperimental pathologyTumor necrosis factor alpha
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H2-M polymorphism in mice susceptible to collagen-induced arthritis involves the peptide binding groove.

1996

The ability to develop type II collagen (CII)-induced arthritis (CIA) in mice is associated with the major histocompatibilityI-A gene and with as yet poorly defined regulatory molecules of the major histocompatibility complex (MHC) class II antigen processing and presentation pathway. H2-M molecules are thought to be involved in the loading of antigenic peptides into the MHC class II binding cleft. We sequencedH2-Ma, H2-Mb1, andH2-Mb2 genes from CIA-susceptible and-resistant mouse strains and identified four differentMa andMb2 alleles and three differentMb1 alleles defined by polymorphic residues within the predicted peptide binding groove. Most CIA-resistant mouse strains share commonMa, M…

musculoskeletal diseasesImmunologyGenes MHC Class IIMolecular Sequence DataGenes MHC Class IPeptide bindingMice Inbred StrainsMajor histocompatibility complexEpitopeMiceAntigenMHC class IGeneticsAnimalsAmino Acid SequencePhylogenyDNA PrimersMHC class IIPolymorphism GeneticbiologyBase SequenceSequence Homology Amino AcidAntigen processingH-2 AntigensHistocompatibility Antigens Class IIMolecular biologyArthritis ExperimentalHistocompatibilityHaplotypesbiology.proteinCollagenSequence AlignmentImmunogenetics
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COX-2 expression in chondrosarcoma: A role for celecoxib treatment?

2010

Chondrosarcomas are resistant to conventional chemo- and radiotherapy. A subset of chondrosarcomas arises secondarily in the benign tumour syndromes enchondromatosis (EC) and multiple osteochondromas (MO), and prevention of tumour development would greatly improve prognosis. We therefore investigated the effect of selective COX-2 inhibition on chondrosarcoma growth. COX-2 expression was studied in central- and peripheral cartilaginous tumours. The effect of COX-2 inhibition was assessed in four high-grade chondrosarcoma cell lines using celecoxib and NS-398 treatment. COX-2 activity (prostaglandin E-2 (PGE(2)) ELISA) and cell viability were measured. The (prophylactic) effect of celecoxib o…

musculoskeletal diseasesMaleCancer ResearchPathologymedicine.medical_specialtyCell Survivalmedicine.medical_treatmentChondrosarcomaDrug Evaluation PreclinicalMice NudeAntineoplastic AgentsBone NeoplasmsMiceIn vivomedicineTumor Cells CulturedAnimalsHumansViability assaySulfonamidesCyclooxygenase 2 Inhibitorsbusiness.industryCartilagemedicine.diseaseXenograft Model Antitumor AssaysRadiation therapyDisease Models Animalmedicine.anatomical_structureOncologyBone tumours Chondrosarcoma COX-2 inhibition Therapy Xenograft familial adenomatous polyposis cell-line cyclooxygenase-2 inhibitor trial tumors establishment emphasis origin boneCell cultureCelecoxibCyclooxygenase 2CelecoxibPyrazolesChondrosarcomabusinessmedicine.drugProstaglandin E
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