Search results for "Type I"

showing 10 items of 966 documents

Activation of cGMP-dependent Protein Kinase Iβ Inhibits Interleukin 2 Release and Proliferation of T Cell Receptor-stimulated Human Peripheral T Cells

2000

Several major functions of type I cGMP-dependent protein kinase (cGK I) have been established in smooth muscle cells, platelets, endothelial cells, and cardiac myocytes. Here we demonstrate that cGK Ibeta is endogenously expressed in freshly purified human peripheral blood T lymphocytes and inhibits their proliferation and interleukin 2 release. Incubation of human T cells with the NO donor, sodium nitroprusside, or the membrane-permeant cGMP analogs PET-cGMP and 8-pCPT-cGMP, activated cGK I and produced (i) a distinct pattern of phosphorylation of vasodilator-stimulated phosphoprotein, (ii) stimulation of the mitogen-activated protein kinases ERK1/2 and p38 kinase, and, upon anti-CD3 stimu…

Blood PlateletsNitroprussideInterleukin 2Cell Membrane PermeabilityCD3 ComplexT-Lymphocytesp38 mitogen-activated protein kinasesT cellReceptors Antigen T-CellCell SeparationBiologyLymphocyte ActivationBiochemistryJurkat cellsJurkat CellsCyclic AMPCyclic GMP-Dependent Protein KinasesmedicineHumansProtein kinase ACyclic GMPMolecular BiologyCyclic GMP-Dependent Protein Kinase Type IKinaseCell growthMicrofilament ProteinsCell BiologyPhosphoproteinsMolecular biologyCell biologyEnzyme ActivationAlternative Splicingmedicine.anatomical_structureInterleukin-2Mitogen-Activated Protein KinasesCell Adhesion MoleculescGMP-dependent protein kinasemedicine.drugJournal of Biological Chemistry
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miR-29b negatively regulates human osteoclastic cell differentiation and function: Implications for the treatment of multiple myeloma-related bone di…

2013

Skeletal homeostasis relies upon a fine tuning of osteoclast (OCLs)-mediated bone resorption and osteoblast (OBLs)-dependent bone formation. This balance is unsettled by multiple myeloma (MM) cells, which impair OBL function and stimulate OCLs to generate lytic lesions. Emerging experimental evidence is disclosing a key regulatory role of microRNAs (miRNAs) in the regulation of bone homeostasis suggesting the miRNA network as potential novel target for the treatment of MM-related bone disease. Here, we report that miR-29b expression decreases progressively during human OCL differentiation in vitro. We found that lentiviral transduction of miR-29b into OCLs, even in the presence of MM cells,…

Bone diseasePhysiologyCellular differentiationCathepsin KClinical BiochemistryGene ExpressionOsteoclastsOsteolysisMMP9Cathepsin KCells CulturedTartrate-resistant acid phosphataseTumorCulturedReceptor Activator of Nuclear Factor-kappa BGenes fosCell DifferentiationOsteoblastCell biologyIsoenzymesmultiple myelomamedicine.anatomical_structureMatrix Metalloproteinase 9osteoclastMatrix Metalloproteinase 2medicine.medical_specialtyfosCellsAcid PhosphataseBiologyCollagen Type IBone resorptionCell LineOsteoclastCell Line TumorInternal medicinemedicineHumansBone ResorptionOsteoblastsmicroRNA.NFATC Transcription FactorsTartrate-Resistant Acid PhosphatasemiR-29bCell Biologymedicine.diseaseActinsMicroRNAsEndocrinologyGenesAcid Phosphatase; Actins; Bone Resorption; Cathepsin K; Cell Differentiation; Cell Line Tumor; Cells Cultured; Collagen Type I; Gene Expression; Genes fos; Humans; Isoenzymes; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; MicroRNAs; Multiple Myeloma; NFATC Transcription Factors; Osteoblasts; Osteoclasts; Osteolysis; Receptor Activator of Nuclear Factor-kappa BJournal of Cellular Physiology
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Serum and urine markers of type I collagen metabolism in elderly women with high and low bone mineral density.

1996

The serum markers of bone formation (carboxy-terminal propeptide of type I collagen, PICP) and resorption (pyridinoline cross-links containing telopeptide of type I collagen, ICTP), as well as urinary resorption markers, pyridinoline (Pyr) and deoxypyridinoline (Dpyr), were studied in 78-year-old women with high (n = 18) and low (n = 17) bone mineral density (BMD) measured from the calcaneus and tibia. The low-BMD group had higher values for PICP (P = 0 center dot 025), Pyr (P = 0 center dot 001) and Dpyr (P < 0 center dot 001) than the high-BMD group. No inverse relationship between these markers and BMD was, however, observed within the study groups. ICTP, Pyr and Dpyr correlated with eac…

Bone mineralmedicine.medical_specialtyDeoxypyridinolineAgingPyridinolineBone densityClinical BiochemistryGeneral Medicinemusculoskeletal systemBiochemistryResorptionBone remodelingchemistry.chemical_compoundEndocrinologychemistryN-terminal telopeptideBone DensityInternal medicinemedicineHumansFemaleCollagenType I collagenAgedEuropean journal of clinical investigation
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Silica as a morphogenetically active inorganic polymer.

2013

At present the scaffolds used for bioprinting of cells do not elicit morphogenetic responses in the cells. In the present study we approached a solution by studying the effect of an inorganic silica supplement added to an Na-alginate matrix. Bone- and osteoblast-like SaOS-2 cells were embedded into this organic polymeric matrix which was additionally enriched with 400 μM prehydrolyzed TEOS [tetra-ethoxy-silane], a source of ortho-silicate. In this silica-based matrix the cells synthesized hydroxyapatite crystallites after exposure to a mineralization activation cocktail composed of β-glycerophosphate, ascorbic acid and dexamethasone. The degree of hydroxyapatite synthesis, determined by sta…

Bone sialoprotein0303 health sciencesbiologyChemistryBiomedical Engineering02 engineering and technology021001 nanoscience & nanotechnologyAscorbic acidMineralization (biology)03 medical and health sciencesstomatognathic systemBiochemistrybiology.proteinOsteocalcinAlkaline phosphataseGeneral Materials ScienceOsteopontinOsteonectin0210 nano-technologyType I collagen030304 developmental biologyBiomaterials science
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Immunohistochemical Evaluation of Periodontal Regeneration Using a Porous Collagen Scaffold.

2021

(1) Aim: To immunohistochemically evaluate the effect of a volume-stable collagen scaffold (VCMX) on periodontal regeneration. (2) Methods: In eight beagle dogs, acute two-wall intrabony defects were treated with open flap debridement either with VCMX (test) or without (control). After 12 weeks, eight defects out of four animals were processed for paraffin histology and immunohistochemistry. (3) Results: All defects (four test + four control) revealed periodontal regeneration with cementum and bone formation. VCMX remnants were integrated in bone, periodontal ligament (PDL), and cementum. No differences in immunohistochemical labeling patterns were observed between test and control sites. N…

Bone sialoproteinPathologyBone RegenerationBiology (General)610 Medicine &amp; healthSpectroscopyDental CementumbiologyTissue ScaffoldsChemistrybiomaterialGeneral MedicineEpithelial cell rests of MalassezComputer Science ApplicationsChemistrymedicine.anatomical_structureimmunohistochemistryKeratinsCollagenPorosityBlood vesselmedicine.medical_specialtyPeriodontal DebridementQH301-705.5Periodontal Ligament610 Medicine & healthvolume-stable collagen matrixCatalysisCollagen Type IArticleInorganic ChemistryhistologyDogsstomatognathic systemProliferating Cell Nuclear Antigenperiodontal regenerationmedicinePeriodontal fiberAnimalsIntegrin-Binding SialoproteinCementumPhysical and Theoretical Chemistryintrabony defectMolecular BiologyQD1-999Regeneration (biology)Organic ChemistryOpen flap debridementcollagen scaffoldHistologybiology.proteinGuided Tissue Regeneration PeriodontalCell Adhesion MoleculesInternational journal of molecular sciences
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Cyclic AMP-mediated upregulation of the expression of neuronal NO synthase in human A673 neuroepithelioma cells results in a decrease in the level of…

2004

The expression level of neuronal nitric oxide synthase (nNOS) can vary depending on the (patho)physiological conditions. Here we document a marked induction of nNOS mRNA, protein, and total NO production in response to dibutyryl cyclic AMP (db-cAMP) in human A673 neuroepithelial cells. However, the upregulation of nNOS was associated with a decreased level of production of bioactive NO and by an increase in the level of generation of reactive oxygen species (ROS). ROS production could be prevented by the NOS inhibitor L-NAME, suggesting nNOS itself is involved in ROS generation. Sepiapterin supplementation of db-cAMP-treated A673 cells could restore full bioactive NO production, most likely…

CAMP-Responsive Element ModulatorNitric Oxide Synthase Type IBiologyCREBNitric OxideBiochemistryAdenylyl cyclaseCyclic AMP Response Element Modulatorchemistry.chemical_compoundMiceNeuroblastomaCoactivatorComplement C3b Inactivator ProteinsCyclic AMPAnimalsHumansNeuroectodermal Tumors Primitive PeripheralCREB-binding proteinEnzyme InhibitorsProtein kinase AeducationCyclic AMP Response Element-Binding ProteinGTP CyclohydrolaseCAMP response element bindingHomeodomain ProteinsNeuronseducation.field_of_studyForskolinPhosphoric Diester HydrolasesIntracellular Signaling Peptides and ProteinsBlood ProteinsLIM Domain ProteinsMolecular biologyCyclic AMP-Dependent Protein KinasesPterinsUp-RegulationDNA-Binding ProteinsRepressor ProteinsAntisense Elements (Genetics)NG-Nitroarginine Methyl EsterchemistryBucladesineGene Expression RegulationComplement Factor Hbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesSignal TransductionBiochemistry
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Upregulation of liver VLDL receptor and FAT/CD36 expressions in LDLR-/- apoB100/100 mice fed trans-10,cis-12 conjugated linoleic acid

2006

International audience; This study explores the mechanisms responsible for the fatty liver setup in mice fed trans-10,cis-12 conjugated linoleic acid (t10c12 CLA), hypothesizing that an induction of low density lipoprotein receptor (LDLR) expression is associated with lipid accumulation. To this end, the effects of t10c12 CLA treatment on lipid parameters, serum lipoproteins, and expression of liver lipid receptors were measured in LDLR(-/-) apoB(100/100) mice as a model of human familial hypercholesterolemia itself depleted of LDLR. Mice were fed t10c12 CLA over 2 or 4 weeks. We first observed that the treatment induced liver steatosis, even in the absence of LDLR. Mice treated for 2 weeks…

CD36 AntigensMaleVery low-density lipoproteinTRANSLOCASECD36RECEPTEUR SCAVENGER[SDV]Life Sciences [q-bio]FATTY ACID TRANSLOCASE030204 cardiovascular system & hematologyBiochemistryMice0302 clinical medicineEndocrinologyLinoleic Acids ConjugatedMice Knockout0303 health sciencesLipoprotein lipaselipoprotéinebiologyacide grasrécepteur d'hormoneChemistryFatty liverFatty Acidsfood and beveragesHEPATIC LIPASELipidsLOW DENSITY LIPOPROTEIN RECEPTOR3. Good healthUp-RegulationLiverSCAVENGER RECEPTOR CLASS B TYPE ILIVER STEATOSIS;LOW DENSITY LIPOPROTEIN RECEPTOR;TRIGLYCERIDE;LIPOATROPHY;LIPOPROTEIN;FATTY ACID TRANSLOCASE;VERY LOW DENSITY LIPOPROTEIN RECEPTOR;HEPATIC LIPASE;LIPOPROTEIN LIPASE;LOW DENSITY LIPOPROTEIN RECEPTOR-RELATED PROTEIN;SCAVENGER RECEPTOR CLASS B TYPE I;LIPOATROPHIE;TRANSLOCASE;LIPASE HEPATIQUE;RECEPTEUR SCAVENGERApolipoprotein B-100lipoprotéine lipaseTRIGLYCERIDElipids (amino acids peptides and proteins)Oxidation-Reductionmedicine.medical_specialtyLIPASE HEPATIQUELipolysisVLDL receptorMice Transgenicacide linoléique conjugué03 medical and health sciencesstéatose hépatiqueInternal medicineLIVER STEATOSISmedicineLIPOPROTEIN LIPASEAnimalsRNA Messengerlipoprotéine de faible densite030304 developmental biologyLOW DENSITY LIPOPROTEIN RECEPTOR-RELATED PROTEINnutritional and metabolic diseasesCell Biologymedicine.diseaseLipid MetabolismLIPOATROPHYDietary FatsEndocrinologyLIPOPROTEINReceptors LDLVERY LOW DENSITY LIPOPROTEIN RECEPTORLIPOATROPHIELDL receptorbiology.proteinacide gras transHepatic lipaseLipoprotein
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Analysis of parathyroid graft rejection suggests alloantigen-specific production of nitric oxide by iNOS-positive intragraft macrophages

2009

Abstract Background During acute rejection of organ or tissue allografts T cells and macrophages are dominant infiltrating cells. CD4-positive T cells are important for the induction of allograft rejection and macrophages are important effector cells mediating cytotoxicity via production of nitric oxide (NO) by the inducible NO-synthase (iNOS). In the present study we analysed whether the destruction of primarily nonvascularised parathyroid allografts is also mediated by iNOS-positive macrophages. Methods Hypocalcaemic Lewis rats received parathyroid isografts (from Lewis donors) and allografts (from Wistar Furth donors), respectively, under the kidney capsule. Levels of serum calcium above…

CD4-Positive T-LymphocytesGraft RejectionMaleImmunologyThyroid GlandNitric Oxide Synthase Type IIRats Inbred WFInflammationCell CommunicationLymphocyte ActivationMajor histocompatibility complexNitric oxidechemistry.chemical_compoundAntigenCell MovementHistocompatibility AntigensmedicineAnimalsTransplantation HomologousImmunology and AllergyCytotoxic T cellMacrophageTransplantationbiologyChemistryMacrophage ActivationAntigens DifferentiationPeptide FragmentsRatsEnzyme ActivationTransplantationMononuclear cell infiltrationGene Expression RegulationRats Inbred LewImmunologyDisease ProgressionMacrophages Peritonealbiology.proteinCalciumImmunizationmedicine.symptomTransplant Immunology
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Nitric oxide enhances Th9 cell differentiation and airway inflammation

2014

International audience; Th9 cells protect hosts against helminthic infection but also mediate allergic disease. Here we show that nitric oxide (NO) promotes Th9 cell polarization of murine and human CD4(+) T cells. NO de-represses the tumour suppressor gene p53 via nitrosylation of Mdm2. NO also increases p53-mediated IL-2 production, STAT5 phosphorylation and IRF4 expression, all essential for Th9 polarization. NO also increases the expression of TGFβR and IL-4R, pivotal to Th9 polarization. OVA-sensitized mice treated with an NO donor developed more severe airway inflammation. Transferred Th9 cells induced airway inflammation, which was exacerbated by NO and blocked by anti-IL-9 antibody.…

CD4-Positive T-LymphocytesInterleukin 2[SDV]Life Sciences [q-bio]Cellular differentiationNitric Oxide Synthase Type IIGeneral Physics and AstronomyMice TransgenicInflammationCell SeparationNitric OxideArticleGeneral Biochemistry Genetics and Molecular BiologyNitric oxideMicechemistry.chemical_compoundEosinophiliaSTAT5 Transcription FactormedicineAnimalsHumansInterleukin 9Cells CulturedInflammationMice Inbred BALB CMultidisciplinarybiologyNitrosylationInterleukin-9Cell DifferentiationGeneral Chemistryrespiratory systemFlow Cytometry3. Good healthCell biologyMice Inbred C57BLchemistryInterferon Regulatory FactorsImmunologyLeukocytes Mononuclearbiology.proteinInterleukin-2Mdm2Tumor Suppressor Protein p53medicine.symptomAntibodymedicine.drugNature Communications
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Antibodies against tumor necrosis factor (TNF) induce T-cell apoptosis in patients with inflammatory bowel diseases via TNF receptor 2 and intestinal…

2011

Background & Aims The anti–tumor necrosis factor (TNF) antibodies infliximab, adalimumab, and certolizumab pegol have proven clinical efficacy in Crohn's disease. Here, we assessed the effects of anti-TNF antibodies on apoptosis in inflammatory bowel disease (IBD). Methods CD14 + macrophages and CD4 + T cells were isolated from peripheral blood and lamina propria mononuclear cells from patients with IBD and control patients. Cell surface markers and apoptosis were assessed by immunohistology and fluorescence-activated cell sorting techniques. Results Lamina propria CD14 + macrophages showed significantly more frequent and higher membrane-bound TNF (mTNF) expression than CD4 + T cells in IBD…

CD4-Positive T-LymphocytesMaleNecrosisCD14Anti-Inflammatory AgentsLipopolysaccharide ReceptorsApoptosisEnzyme-Linked Immunosorbent AssayBiologyAntibodies Monoclonal HumanizedReal-Time Polymerase Chain ReactionPeripheral blood mononuclear cellPolyethylene GlycolsImmunoglobulin Fab FragmentsYoung AdultmedicineHumansReceptors Tumor Necrosis Factor Type IIAntigen-presenting cellAgedLamina propriaHepatologyCluster of differentiationTumor Necrosis Factor-alphaMacrophagesGastroenterologyAdalimumabAntibodies MonoclonalMiddle AgedFlow CytometryInflammatory Bowel DiseasesInfliximabmedicine.anatomical_structureApoptosisCase-Control StudiesImmunologyCertolizumab PegolTumor necrosis factor alphaFemalemedicine.symptomGastroenterology
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