Search results for "messenger"

showing 10 items of 1493 documents

Production of reactive oxygen intermediates by human macrophages exposed to soot particles and asbestos fibers and increase in NF-kappa B p50/p105 mR…

1999

Alveolar macrophages (AM) play a decisive role in the immunologic defense system of the lung and in inflammatory pulmonary pathomechanisms. AM and blood monocytes (BM) were exposed to chrysotile B, soot FR 101, and Printex 90 (P 90). We evaluated the reactive oxygen intermediate (ROI) release of AM and BM after particle exposure. ROI release was measured by chemiluminescence. Thirty-minute exposure caused a significant (up to 2.5-fold) increase in ROI release of AM (100 micrograms/10(6) cells) compared with control experiments (p0.01). Identical exposure conditions for BM resulted in a similar reaction pattern (maximum 2.2-fold increase in ROI release; p0.05). After a 90-min particle exposu…

Pulmonary and Respiratory MedicineAdultMaleP50Asbestos Serpentinemedicine.medical_treatmentMonocytesProinflammatory cytokineSuperoxide dismutaseGene expressionMacrophages AlveolarmedicineHumansRNA MessengerReceptorCells CulturedAgedLungbiologyDose-Response Relationship DrugChemistryReverse Transcriptase Polymerase Chain ReactionNF-kappa BMiddle AgedNFKB1Molecular biologyCarbonCytokinemedicine.anatomical_structureGene Expression RegulationImmunologyLuminescent Measurementsbiology.proteinFemaleReactive Oxygen SpeciesBronchoalveolar Lavage FluidLung
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The host defence peptide LL-37/hCAP-18 is a growth factor for lung cancer cells

2007

Cancer development can be viewed as dysregulated repair. Antimicrobial peptides (AMPs) are effector molecules of the innate immune system with direct antimicrobial activity. Beside this host defence function several AMPs play a role in the regulation of inflammation and tissue repair. The aim of the present study was to investigate whether the human cathelicidin AMP LL-37/hCAP-18 is involved in the biology of lung cancer. Human cancer cell lines were found to express the human cathelicidin LL-37/hCAP-18 mRNA and peptide at different levels. Immunohistochemistry of human lung cancers showed that the peptide is expressed mostly in adenocarcinoma and squamous cell carcinoma. Application of exo…

Pulmonary and Respiratory MedicineCancer ResearchLung Neoplasmsmedicine.medical_treatmentMice NudeBiologyCathelicidinMiceCathelicidinsCell Line TumormedicineAnimalsHumansRNA MessengerEpidermal growth factor receptorGrowth SubstancesLung cancerMice Inbred BALB CInnate immune systemCell growthGrowth factorCancermedicine.diseaseErbB ReceptorsOncologyCell cultureImmunologyCancer researchbiology.proteinFemaleAntimicrobial Cationic PeptidesSignal TransductionLung Cancer
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Cigarette smoke exposure inhibits extracellular MMP-2 (gelatinase A) activity in human lung fibroblasts

2007

Abstract Background Exposure to cigarette smoke is considered a major risk factor for the development of lung diseases, since its causative role has been assessed in the induction and maintenance of an inflamed state in the airways. Lung fibroblasts can contribute to these processes, due to their ability to produce proinflammatory chemotactic molecules and extracellular matrix remodelling proteinases. Among proteolytic enzymes, gelatinases A and B have been studied for their role in tissue breakdown and mobilisation of matrix-derived signalling molecules. Multiple reports linked gelatinase deregulation and overexpression to the development of inflammatory chronic lung diseases such as COPD.…

Pulmonary and Respiratory MedicineGelatinase ABiologyMatrix metalloproteinaseProinflammatory cytokineExtracellular matrixExtracellularHumansGelatinaseRNA MessengerLungCells Culturedlcsh:RC705-779Cell DeathPlant ExtractsResearchProteolytic enzymessmoke MMP-2Tissue Inhibitor of MetalloproteinasesEnvironmental Exposurelcsh:Diseases of the respiratory systemEnvironmental exposureFibroblastsrespiratory systemrespiratory tract diseasesCulture Media ConditionedImmunologyMatrix Metalloproteinase 2Tobacco Smoke PollutionEnvironmental MonitoringRespiratory Research
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Indoor air pollutants stimulate interleukin-8-specific mRNA expression and protein secretion of alveolar macrophages.

1998

Indoor air pollutants may cause inflammatory changes of the airways and adjacent pulmonary tissue. After phagocytosis of inhaled particles alveolar macrophages (AM) release chemotactic mediators capable of attracting inflammatory cells into the lung tissue. To evaluate these mechanisms further peripheral blood mononuclear cells (PBMNC) and human AM (freshly recovered from the lower respiratory tract) were exposed to the indoor particles Soot FR 101 and Printex 90, the asbestos fiber Chrysotile B, and titanium dioxide (TiO2) at concentrations of 10 or 50 microg/10(6) cells for up to 8 h. The migration of granulocytes into the conditioned supernatants of AM and PBMNC was quantified by chemota…

Pulmonary and Respiratory MedicineGranulocyte migrationAdultMaleChemokineBiologyGranulocytePeripheral blood mononuclear cellPolymerase Chain ReactionMicrobiologyMacrophages AlveolarmedicineHumansInterleukin 8RNA MessengerAgedAir PollutantsLungInterleukin-8InterleukinMolecular biologyChemotaxis Leukocytemedicine.anatomical_structureAir Pollution Indoorbiology.proteinLeukocytes MononuclearFemaleBronchoalveolar Lavage FluidChemotaxis assayLung
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Interleukin-2 receptor gene expression by bronchoalveolar lavage lymphocytes in pulmonary sarcoidosis.

1989

Current concepts of the immunopathogenesis of sarcoidosis favor a central role of activated, interleukin-2 (IL-2) producing helper T-cells at sites of inflammation. Normally, activated T-cells release IL-2 and express IL-2 receptors (IL-2R). IL-2R+ cells, however, are not uniformly found in patients with clinically active disease. To determine whether the lack of IL-2R+ cells is caused by a dysregulation of the IL-2R gene or by the mode of T-cell activation in pulmonary sarcoidosis, we quantified IL-2 and IL-2R m-RNA transcripts, IL-2 release, and IL-2R surface protein in peripheral blood lymphocytes of patients with sarcoidosis and normal control subjects before and after in vitro stimulat…

Pulmonary and Respiratory MedicineInterleukin 2AdultLung DiseasesPathologymedicine.medical_specialtySarcoidosisLymphocyteT-LymphocytesInflammationLymphocyte ActivationIn vivomedicineHumansRNA MessengerReceptorLungmedicine.diagnostic_testbusiness.industryReceptors Interleukin-2medicine.diseasemedicine.anatomical_structureBronchoalveolar lavageGene Expression RegulationImmunologyInterleukin-2Sarcoidosismedicine.symptombusinessBronchoalveolar Lavage Fluidmedicine.drugThe American review of respiratory disease
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Long non-coding RNA and messenger RNA—the meeting of two worlds

2018

Long non-coding RNAs (lncRNAs), defined as transcripts without protein-coding potential, have recently emerged as key mediators in numerous biological functions. LncRNAs act as regulators of gene expression at different levels including transcriptional and post-transcriptional regulation as well as chromatin organization.

Pulmonary and Respiratory MedicineMessenger RNAEditorialbusiness.industryGene expressionMedicineComputational biologybusinessLong non-coding RNAChromatinJournal of Thoracic Disease
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Chronological expression of Ciliated Bronchial Epithelium 1 during pulmonary development

2009

Ciliated Bronchial Epithelium (CBE) 1 is a novel gene, which is expressed in ciliated cells. As cilia are important during embryogenesis, the present authors characterised the murine homologue of CBE1 (Cbe1) and compared its temporal expression during murine and human lung development. Cbe1 cDNA was cloned and characterised using sequencing, standard PCR and Western blotting. Mouse and human embryonic/fetal lungs (HELs) were harvested for mRNA analysis and protein localisation in vivo and in vitro using RT-PCR and immunohistochemistry. The Cbe1 amino acid sequence was >75% identical with CBE1 and its alternative splicing and tissue distribution were highly conserved. Pulmonary expression of…

Pulmonary and Respiratory MedicinePathologymedicine.medical_specialtyDNA ComplementaryTime FactorsBlotting WesternDNA Mutational AnalysisBiologyTransfectionStatistics NonparametricImmunoenzyme TechniquesMiceOpen Reading FramesCiliogenesisGene expressionmedicineAnimalsHumansAmino Acid SequenceRNA MessengerCloning MolecularLungDNA PrimersFetusMessenger RNALungReverse Transcriptase Polymerase Chain ReactionEmbryogenesisAlternative splicingNuclear ProteinsCell DifferentiationMolecular biologyEpitheliumDNA-Binding Proteinsmedicine.anatomical_structureBronchial epithelium Asthma DevelopmentTranscription FactorsEuropean Respiratory Journal
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Induction of stress proteins in human endothelial cells by heavy metal ions and heat shock.

1999

In the present study, we compared the induction of heat shock proteins (HSPs) by heat and heavy metal ions in three different endothelial cell types, namely, human umbilical vein endothelial cells, human pulmonary microvascular endothelial cells, and the cell line EA.hy 926. Our results show that especially Zn2+and Cd2+are inducers of 70-kDa (HSP70), 60-kDa (HSP60), 32-kDa (HSP32), and 27-kDa (HSP27) HSPs. The strength of inducibility is specific for each HSP. Ni2+and Co2+only show an inducible effect at very high concentrations, that is, in the clearly cytotoxic range. Furthermore, we investigated the time course of HSP expression and the involvement of heat shock factor-1. Our study demon…

Pulmonary and Respiratory MedicineUmbilical VeinsPhysiologyMetal ions in aqueous solutionBlotting WesternGene ExpressionBiologyUmbilical veinPhysiology (medical)Heat shock proteinMetals HeavyGene expressionmedicineHumansHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsRNA MessengerFluorescent Antibody Technique IndirectCells CulturedHeat-Shock ProteinsCell BiologyChaperonin 60Endothelial stem cellmedicine.anatomical_structureCell cultureShock (circulatory)ImmunologyBiophysicsEndothelium Vascularmedicine.symptomHeat-Shock ResponseBlood vesselThe American journal of physiology
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Aclidinium inhibits human lung fibroblast to myofibroblast transition

2011

Background Fibroblast to myofibroblast transition is believed to contribute to airway remodelling in lung diseases such as asthma and chronic obstructive pulmonary disease. This study examines the role of aclidinium, a new long-acting muscarinic antagonist, on human fibroblast to myofibroblast transition. Methods Human bronchial fibroblasts were stimulated with carbachol (10 −8 to 10 −5  M) or transforming growth factor-β1 (TGF-β1; 2 ng/ml) in the presence or absence of aclidinium (10 −9 to 10 −7  M) or different drug modulators for 48 h. Characterisation of myofibroblasts was performed by analysis of collagen type I and α-smooth muscle actin (α-SMA) mRNA and protein expression as well as α…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyCarbacholChronic Obstructive Pulmonary DiseaseBronchiMuscarinic AntagonistsBiologyCholinergic AgonistsCollagen Type ITransforming Growth Factor beta1Downregulation and upregulationWestern blotanticholinergicCell MovementInternal medicinemedicineCOPDHumans1506RNA MessengerAutocrine signallingFibroblastMyofibroblastsCells CulturedCell Proliferationmedicine.diagnostic_testDose-Response Relationship Drugairway epitheliumCell Differentiationasthmainterstitial fibrosisFibroblastsAdenosineMolecular biologymyofibroblastActinsUp-RegulationEndocrinologymedicine.anatomical_structurePhosphorylationFibroblastCarbacholMyofibroblastmedicine.drugTropanesThorax
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GABAC receptors are functionally expressed in the intermediate zone and regulate radial migration in the embryonic mouse neocortex

2010

Radial neuronal migration in the cerebral cortex depends on trophic factors and the activation of different voltage- and ligand-gated channels. To examine the func- tional role of GABAC receptors in radial migration we ana- lyzed the effects of specific GABAA and GABAC receptor antagonists on the migration of BrdU-labeled neurons in vitro using organotypic neocortical slice cultures. These experi- ments revealed that the GABAA specific inhibitor bicuculline methiodide facilitated neuronal migration, while the GABAC specific inhibitor (1,2,5,6-tetrahydropyridine-4-yl) methylphos- phinic-acid (TPMPA) impeded migration. Co-application of TPMPA and bicuculline methiodide or the unspecific ionot…

PyridinesNeocortexIn Vitro TechniquesBiologyBicucullineGABAA-rho receptorGABA AntagonistsMicechemistry.chemical_compoundReceptors GABACell MovementmedicineAnimalsPicrotoxinGABA-A Receptor AntagonistsRNA MessengerReceptorGABA AgonistsNeuronsNeocortexGABAA receptorGeneral NeuroscienceGABA receptor antagonistReceptors GABA-APhosphinic AcidsCell biologyMice Inbred C57BLmedicine.anatomical_structurechemistryCrotonatesGABAergicNeurosciencePicrotoxinIonotropic effectNeuroscience
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