Search results for "kinases"

showing 10 items of 929 documents

2′O-galloylhyperin attenuates LPS-induced acute lung injury via up-regulation antioxidation and inhibition of inflammatory responses in vivo

2019

2'O-galloylhyperin, an active flavonol glycoside compound with remarkable anti-immune activity, was isolated from Pyrola [P. incarnata Fisch.]. However, the evidence of anti-inflammatory activity in pulmonary diseases was still not convincing. The aim of the present study was (1) to investigate the effect of 2'O-galloylhyperin on LPS-induced acute lung injury in mice, and (2) to identify the mechanisms of attenuation of inflammatory responses. The results demonstrated that 2'O-galloylhyperin significantly reduced LPS-induced inflammation damage in a dose-dependent manner. After LPS challenge, treatment with 2'O-galloylhyperin reduced the production of pro-inflammatory cytokines and chemokin…

LipopolysaccharidesMale0301 basic medicineMAPK/ERK pathwayp38 mitogen-activated protein kinasesAcute Lung InjuryMolecular ConformationInflammationPharmacologyLung injuryToxicologyAntioxidantsMiceStructure-Activity Relationship03 medical and health sciences0302 clinical medicineGallic AcidmedicineAnimalsProtein kinase AInflammationMice Inbred ICRDose-Response Relationship DrugChemistryAnti-Inflammatory Agents Non-SteroidalAMPKGeneral MedicineUp-Regulation030104 developmental biology030220 oncology & carcinogenesisPhosphorylationQuercetinmedicine.symptomSignal transductionChemico-Biological Interactions
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Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
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Identification and characterization of a novel Ets-2-related nuclear complex implicated in the activation of the human interleukin-12 p40 gene promot…

1997

Interleukin-12 (IL-12) is a proinflammatory cytokine produced by antigen-presenting cells in response to many microbial infections. IL-12 plays an important role in the generation of T helper type-1 cells, which favor cell-mediated immune response. IL-12 is composed of two different subunits, p40 and p35, whose expression can be regulated concomitantly or differentially. Monocytic cells, the major producers of IL-12, can be primed by interferon-gamma (IFN-gamma) to produce optimal amounts of IL-12 in response to LPS stimulation as a consequence of bacterial infection. The priming effect is exerted primarily at the transcriptional level on the p40 promoter in conjunction with the effects of …

LipopolysaccharidesTranscription GeneticSequence HomologyStimulationbiosynthesis/geneticsBiochemistryChromatography Affinitychemistry.chemical_compoundMiceAnimals Base Sequence Cell Line Cell Nucleus; metabolism Chromatography; Affinity DNA-Binding Proteins Humans Interferon-gamma; pharmacology Interleukin-12; biosynthesis/genetics Kinetics Lipopolysaccharides; pharmacology Mice Molecular Sequence Data Nuclear Proteins; isolation /&/ purification/metabolism Promoter Regions; Genetic Protein-Tyrosine Kinases; metabolism Proto-Oncogene Protein c-ets-2 Proto-Oncogene Proteins; isolation /&/ purification/metabolism Repressor Proteins Sequence Homology; Nucleic Acid Trans-Activators; isolation /&/ purification/metabolism Transcription Factors Transcription; Genetic; drug effectsPromoter Regions GeneticChromatographyNuclear ProteinsMethylationProtein-Tyrosine KinasesInterleukin-12DNA-Binding ProteinsTranscriptionMolecular Sequence DataBiologyProinflammatory cytokineCell LineProto-Oncogene Protein c-ets-2Promoter RegionsInterferon-gammaGeneticSequence Homology Nucleic AcidProto-Oncogene ProteinsAnimalsHumansMolecular BiologyTranscription factorCell NucleusMolecular massBase SequenceNucleic Acidisolation /&/ purification/metabolismPromoterCell BiologyMolecular biologyIn vitroRepressor ProteinsKineticschemistryAffinitydrug effectsTrans-ActivatorspharmacologymetabolismDNATranscription Factors
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Inflammatory Characteristics of Monocytes from Pediatric Patients with Tuberous Sclerosis.

2015

Objective  Therapeutic options for the tuberous sclerosis complex (TSC) syndrome showed varying outcomes. Malfunctional tsc1 / tsc2 genes leave mTOR uninhibited, a positive downstream modulator of the innate proinflammatory immune system, which has not yet been described in pediatric patients with TSC. Methods  Using polymerase chain reaction (PCR) gene expression levels of monocytes after cultivation with lipopolysaccharide (LPS) or with LPS + mTOR inhibitor rapamycin, patients with TSC ( n  = 16) were compared with healthy subjects ( n  = 20). Results  Compared with monocytes from healthy controls, LPS showed a more prominent gene expression pattern in patients with TSC (CCL24, CXCL10, IL…

Lipopolysaccharidescongenital hereditary and neonatal diseases and abnormalitiesLipopolysaccharideGene ExpressionMonocytesProinflammatory cytokinechemistry.chemical_compoundTuberous sclerosisTuberous SclerosisGene expressionmedicineCXCL10HumansChildInflammationSirolimusbusiness.industryTOR Serine-Threonine KinasesInfant NewbornInfantGeneral Medicinemedicine.diseasemedicine.anatomical_structureCross-Sectional StudieschemistryChild PreschoolPediatrics Perinatology and Child HealthImmunologyCytokinesNeurology (clinical)TSC1TSC2Inflammation MediatorsbusinessCCL24Immunosuppressive AgentsNeuropediatrics
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Acute exercise activates nuclear factor (NF)-kappaB signaling pathway in rat skeletal muscle.

2004

Two studies were performed to investigate the effects of an acute bout of physical exercise on the nuclear protein kappaB (NF-kappaB) signaling pathway in rat skeletal muscle. In Study 1, a group of rats (n=6) was run on the treadmill at 25 m/min, 5% grade, for 1 h or until exhaustion (Ex), and compared with a second group (n=6) injected with two doses of pyrrolidine dithiocarbamate (PDTC, 100 mg/kg, i.p.) 24 and 1 h prior to the acute exercise bout. Three additional groups of rats (n=6) were injected with either 8 mg/kg (i.p.) of lipopolysaccharide (LPS), 1 mmol/kg (i.p.) t-butylhydroperoxide (tBHP), or saline (C) and killed at resting condition. Ex rats showed higher levels of NF-kappaB b…

Lipopolysaccharidesmedicine.medical_specialtyP50PyrrolidinesElectrophoretic Mobility Shift AssayIκB kinaseBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeBiochemistryRats Sprague-Dawleychemistry.chemical_compoundPyrrolidine dithiocarbamateNF-KappaB Inhibitor alphatert-ButylhydroperoxideThiocarbamatesInternal medicinePhysical Conditioning AnimalGeneticsmedicineAnimalsMuscle SkeletalMolecular Biologychemistry.chemical_classificationReactive oxygen speciesNF-kappa BSkeletal muscleI-kappa B KinaseRatsCytosolOxidative Stressmedicine.anatomical_structureEndocrinologychemistryFemaleI-kappa B ProteinsSignal transductionOxidative stressBiotechnologySignal TransductionFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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The antifibrotic potential of a sustained release formulation of a PDGF beta-receptor targeted rho kinase inhibitor

2019

Rho kinase activity in hepatic stellate cells (HSCs) is associated with activation, transformation and contraction of these cells, leading to extracellular matrix production and portal hypertension in liver cirrhosis. Inhibition of rho kinase activity can reduce these activities, but may also lead to side effects, for instance systemic hypotension. This can be circumvented by liver-specific delivery of a rho kinase inhibitor to effector cells. Therefore, we targeted the rho kinase inhibitor Y27632 to the key pathogenic cells in liver fibrosis, i.e. myofibroblasts including activated HSCs that highly express the PDGF beta-receptor, using the drug carrier pPB-MSA. This carrier consists of mou…

Liver CirrhosisDrug targetingPyridinesPolymeric microspheresPharmaceutical Science02 engineering and technologyPharmacologychemistry.chemical_compoundY-27632FibrosisControlled releaseRho-associated protein kinaseMice Knockout0303 health sciencesDrug Carriersrho-Associated KinasesChemistryCIRRHOTIC RATS021001 nanoscience & nanotechnologyMicrospheresY-27632Drug deliveryFemale0210 nano-technologyDrug carrierATP Binding Cassette Transporter Subfamily BSIGNALING CONTRIBUTESLiver fibrosisBiologicalsHEPATIC STELLATE CELLSCell LineMECHANISMSReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesDELIVERYROCK INHIBITORmedicineAnimalsHumansProtein Kinase Inhibitors030304 developmental biologyProtein deliveryPORTAL PRESSUREmedicine.diseaseAmidesTargeted drug deliveryRho kinase inhibitorDelayed-Action PreparationsHepatic stellate cellVASODILATIONJournal of Controlled Release
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MERTK rs4374383 polymorphism affects the severity of fibrosis in non-alcoholic fatty liver disease

2015

Background & Aim Homozygosity for a common non-coding rs4374383 G>A polymorphism in MERTK (myeloid-epithelial-reproductive tyrosine kinase) has been associated with the protection against fibrosis progression in chronic hepatitis C. The main study objective was to assess whether MERTK AA genotype influences liver fibrosis, and secondarily MERTK expression in patients with non-alcoholic fatty liver disease (NAFLD). We also investigated whether MERTK is expressed in human hepatic stellate cells (HSC) and in murine models of fibrogenesis. Methods We considered 533 consecutive patients who underwent liver biopsy for suspected non-alcoholic steatohepatitis (NASH) without severe obesity from two …

Liver CirrhosisMale0301 basic medicineMessengerMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisInbred BALB CCells CulturedMice Inbred BALB CCulturedmedicine.diagnostic_testMedicine (all)Fatty liverNASHMiddle AgedLiver biopsyFemale030211 gastroenterology & hepatologyAdultmedicine.medical_specialtyMERTKCellsBiology03 medical and health sciencesGeneticProto-Oncogene ProteinsInternal medicinemedicineAnimalsHumansFibrosis; MERTK; NASH; Adult; Animals; Cells Cultured; Female; Humans; Liver Cirrhosis; Male; Mice Inbred BALB C; Middle Aged; Non-alcoholic Fatty Liver Disease; Proto-Oncogene Proteins; RNA Messenger; Receptor Protein-Tyrosine Kinases; Polymorphism Genetic; Medicine (all); HepatologyRNA MessengerPolymorphismPolymorphism Geneticc-Mer Tyrosine KinaseHepatologyGAS6Receptor Protein-Tyrosine Kinasesnafld fibrosis mertkMERTKHepatologymedicine.diseaseFibrosis030104 developmental biologyImmunologyHepatic stellate cellRNASteatohepatitisJournal of Hepatology
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Increased hepatic fibrosis and JNK2-dependent liver injury in mice exhibiting hepatocyte-specific deletion of cFLIP.

2012

Chronic liver disease promotes hepatocellular injury involving apoptosis and triggers compensatory regeneration that leads to the activation of quiescent stellate cells in the liver. The deposition of extracellular matrix from activated myofibroblasts promotes hepatic fibrosis and the progression to cirrhosis with deleterious effects on liver physiology. The role of apoptosis signaling pathways in the development of fibrosis remains undefined. The aim of the current study was to determine the involvement of the caspase-8 homologue cellular FLICE-inhibitory protein (cFLIP) during the initiation and progression of fibrosis. Liver injury and fibrosis from carbon tetrachloride (CCl4) and thioa…

Liver CirrhosisMalePathologymedicine.medical_specialtyTime FactorsGenotypePhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBiologyThioacetamideChronic liver diseaseMicePhysiology (medical)medicineAnimalsMitogen-Activated Protein Kinase 9PhosphorylationExtracellular Signal-Regulated MAP KinasesCarbon TetrachlorideCompensatory regenerationLiver injuryMice KnockoutHepatologyCaspase 3Gastroenterologymedicine.diseaseCaspase 9Enzyme ActivationDisease Models Animalmedicine.anatomical_structurePhenotypeLiverApoptosisHepatocyteHepatic stellate cellCancer researchDisease ProgressionHepatocytesHepatocellular injuryChemical and Drug Induced Liver InjuryHepatic fibrosisSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
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Mer Tyrosine Kinase (MERTK) modulates liver fibrosis progression and hepatocellular carcinoma development.

2022

BackgroundMerTK is a tyrosine kinase receptor that belongs to the TAM (Tyro3/Axl/Mer) receptor family. It is involved in different processes including cellular proliferation/survival, cellular adhesion/migration, and release of the inflammatory/anti-inflammatory cytokines. Although it is reported that MERTK polymorphisms affect the severity of viral and metabolic liver diseases, being able to influence fibrosis progression and hepatocellular carcinoma development, the mechanisms remain unknown. Methods: using a microarray approach, we evaluated the liver expression of genes involved in fibrogenesis and hepatocarcinogenesis in patient with chronic hepatitis C (CHC), stratified for MERTK geno…

Liver CirrhosisSettore MED/12 - GastroenterologiaCarcinoma Hepatocellularc-Mer Tyrosine KinaseMer Tyrosine Kinase polymorphism (MERTK polymorphism) WNT gene family pathway (WNT pathway) hepatocellular carcinoma liver fibrosis matrix metallopeptidase Metalloproteases Protein-Tyrosine Kinases Liver CirrhosisImmunologyLiver NeoplasmsProtein-Tyrosine KinasesFibrosisSettore BIO/13 - Biologia ApplicataProto-Oncogene ProteinsMetalloproteasesImmunology and AllergyHumansFrontiers in immunology
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Sphingosine-1-phosphate increases human alveolar epithelial IL-8 secretion, proliferation and neutrophil chemotaxis

2009

Sphingosine-1-phosphate (S1P) has been presented recently as a pro-inflammatory agent in the airway epithelium since S1P levels are increased in bronchoalveolar lavage fluid of human asthmatics. However, the effects of S1P over the alveolar epithelium and neutrophil interactions are poorly understood. Here, we show that S1P increased interleukin 8 (IL-8) gene expression and protein secretion and proliferation in alveolar epithelial cells A549 at physiological concentrations (1 microM). At the same time, S1P increased intracellular Ca2+ concentration (potency 17.91 microM, measured by epifluorescence microscopy), phospholipase D (PLD) activity (measured by chemiluminiscence method) and extra…

LuminescenceNeutrophilsIntercellular Adhesion Molecule-1Gene ExpressionBiologyPertussis toxinReceptors G-Protein-Coupled1-ButanolSphingosineCell Line TumorPhospholipase DHumansInterleukin 8PhosphorylationExtracellular Signal-Regulated MAP KinasesEgtazic AcidCell ProliferationFlavonoidsPharmacologyA549 cellCell adhesion moleculeInterleukin-8Epithelial CellsChemotaxisIntercellular Adhesion Molecule-1Intercellular adhesion moleculeMolecular biologyPulmonary AlveoliChemotaxis LeukocytePertussis ToxinBiochemistryRespiratory epitheliumCalciumlipids (amino acids peptides and proteins)LysophospholipidsEuropean Journal of Pharmacology
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