Search results for "p38 mitogen-activated protein kinases"

showing 10 items of 145 documents

Age-dependent regulation of antioxidant genes by p38α MAPK in the liver

2018

p38α is a redox sensitive MAPK activated by pro-inflammatory cytokines and environmental, genotoxic and endoplasmic reticulum stresses. The aim of this work was to assess whether p38α controls the antioxidant defense in the liver, and if so, to elucidate the mechanism(s) involved and the age-related changes. For this purpose, we used liver-specific p38α-deficient mice at two different ages: young-mice (4 months-old) and old-mice (24 months-old). The liver of young p38α knock-out mice exhibited a decrease in GSH levels and an increase in GSSG/GSH ratio and malondialdehyde levels. However, old mice deficient in p38α had higher hepatic GSH levels and lower GSSG/GSH ratio than young p38α knock-…

ROS Reactive oxygen species;RSK1 Ribosomal S6 kinase10301 basic medicineMAPK/ERK pathwayAgingHPLC High-performance liquid chromatographyAntioxidantmedicine.medical_treatmentTBP TATA-binding proteinClinical BiochemistryDEN Diethyl nitrosamine;MKP-1 MAPK phosphatase-1IκB kinaseGCLc Glutamate cysteine ligase catalytic subunitp38 Mitogen-Activated Protein KinasesG6PDH Glucose-6-phosphate dehydrogenaseBiochemistryAntioxidantsMicechemistry.chemical_compoundSuperoxide Dismutase-1Akt Protein kinase B0302 clinical medicineNrf2 Nuclear factor erythroid 2-related factor-2IL InterleukinSOD1 Cu/Zn-superoxide dismutaselcsh:QH301-705.5Mice KnockoutMK2 MAP-activated protein kinase 2;PGC-1α Peroxisome proliferator-activated receptor gamma coactivator 1-alphachemistry.chemical_classificationlcsh:R5-920Trx ThioredoxinGlutathione DisulfideTNF-α Tumor necrosis factor-alphabiologyLPS Lipopolysaccharide;GSSG Oxidized glutathione;MEF Mouse embryonic fibroblastsNF-kappa BGstm1 Glutathione S-transferase mu 1CatalaseEndoplasmic Reticulum StressGlutathioneLiverGSH Reduced glutathione;Catalase030220 oncology & carcinogenesisJNK c-Jun N-terminal kinaselcsh:Medicine (General)Research Papermedicine.medical_specialtyNF-E2-Related Factor 2Glutamate-Cysteine LigaseMKK MAPK kinaseAP-1 Activator protein-1IKK IƙB KinaseGene Expression Regulation EnzymologicSuperoxide dismutase03 medical and health sciencesInternal medicineGlutamate cysteine ligaseEGFR Epidermal growth factor receptormedicineAnimalsNuclear factor ƙBAnd catalaseChIP Chromatin immunoprecipitation;Protein kinase BNF-ƙB Nuclear factor kappa BSuperoxide DismutaseSuperoxide dismutase 1Superoxide dismutase 2Organic ChemistryGlutathioneASK1 Apoptosis signal-regulating kinase 1ATF2 activating transcription factor 2;030104 developmental biologyEndocrinologyEnzymeHsp Heat shock proteinlcsh:Biology (General)chemistrybiology.proteinSOD2 Mn-superoxide dismutaseMAPK mitogen activated protein kinaseNEM N-ethyl maleimide;Redox Biology
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Decreased SAPK/JNK signalling affects cytokine release and STAT3 activation in psoriatic fibroblasts.

2015

STAT3 Transcription FactorMAP Kinase Signaling Systemmedicine.medical_treatmentDermatologyBiochemistryp38 Mitogen-Activated Protein KinasesPsoriasismedicineSapk jnkHumansPsoriasisPhosphorylationSTAT3Molecular BiologyStat3 activationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyChemistryInterleukin-6Tumor Necrosis Factor-alphaInterleukin-8JNK Mitogen-Activated Protein KinasesTranscription Factor RelAFibroblastsmedicine.diseaseSignallingCytokineCase-Control StudiesCancer researchbiology.proteinPhosphorylationTumor necrosis factor alphaExperimental dermatology
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Intestinal anti-inflammatory activity of ellagic acid in the acute and chronic dextrane sulfate sodium models of mice colitis.

2013

Abstract Ethnopharmacological relevance Pomegranate (Punica granatum L.; Lythraceae) has traditionally been used for the treatment of various inflammatory diseases, including ulcerative colitis (UC). Because its fruits and extracts are rich in ellagitannins, which release ellagic acid when hydrolyzed, consumption of pomegranate products is currently being widely promoted for their potential health effects, including the prevention of inflammatory diseases and cancer. To evaluate the anti-inflammatory effects of ellagic acid on dextran sulfate sodium (DSS)-induced acute and chronic experimental colitis in two different strains of mice and to elucidate its possible mechanisms of action. Mater…

STAT3 Transcription Factormedicine.drug_classColonp38 mitogen-activated protein kinasesAnti-Inflammatory AgentsPharmacologyp38 Mitogen-Activated Protein KinasesAnti-inflammatoryBALB/cchemistry.chemical_compoundMiceEllagic AcidNF-KappaB Inhibitor alphaDrug DiscoverymedicineAnimalsColitisIntestinal MucosaSTAT3PeroxidasePharmacologyMice Inbred BALB Cbiologybusiness.industryDextran SulfateNF-kappa BCancermedicine.diseasebiology.organism_classificationColitisUlcerative colitisMice Inbred C57BLDisease Models AnimalchemistryImmunologybiology.proteinCytokinesFemaleI-kappa B ProteinsbusinessEllagic acidJournal of ethnopharmacology
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Post-Transcriptional Regulation of Human Inducible Nitric-Oxide Synthase Expression by the Jun N-terminal Kinase

2007

Human inducible nitric-oxide synthase (iNOS) expression is regulated both at transcriptional and post-transcriptional levels. In the present study, the effect of Jun N-terminal kinase (JNK) on human iNOS expression was investigated. In A549/8 human alveolar epithelial cells, both the inhibition of JNK by a pharmacological inhibitor anthra[1,9-cd]pyrazol-6(2H)-one1,9-pyrazoloanthrone (SP600125) and small interfering RNA (siRNA)-mediated down-regulation of JNK led to a reduction of iNOS mRNA and protein expression. iNOS promoter activity was not affected by these treatments. Hence, JNK seems to regulate iNOS expression through post-transcriptional mechanisms by stabilizing iNOS mRNA. Our labo…

Small interfering RNARNA Stabilityp38 mitogen-activated protein kinasesDown-RegulationNitric Oxide Synthase Type IIRNA-binding proteinNitric Oxidep38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicCell LineTristetraprolinHumansPhosphorylationRNA Small InterferingPromoter Regions GeneticPost-transcriptional regulationAnthracenesPharmacologyRegulation of gene expressionMessenger RNAbiologyChemistryKinaseJNK Mitogen-Activated Protein KinasesEpithelial Cellsrespiratory systemMolecular biologyPulmonary AlveoliNitric oxide synthasebiology.proteinCytokinesMolecular MedicineSignal TransductionMolecular Pharmacology
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p38 MAPK activation is required for Paracentrotus lividus skeletogenesis

2008

We investigated the p38 MAPK role during sea urchin, Paracentrotus lividus, development. We found that at the morula stage, before the onset of skeletogenesis, p38 MAPK shows a peak of activity, and we tested whether p38 MAPK activity has any effect on skeletogenesis. By immunohistochemistry on whole-mount embryos we show the preferential localization of the active p38 form both in the presumptive PMCs and bilateral spiculo- genesis centers in control embryos, and in the radialized supernumerary spiculogenesis centers induced by NiCl2 treatment. By using SB203580, a p38 MAPK specific inhibitor, we show that p38 activity is required both for the initial triradiate spicule rudiments formation…

Spiculeanimal structuresbiologyp38 mitogen-activated protein kinasesEmbryoAnatomyp38 MAPKbiology.organism_classificationSB203580Paracentrotus lividusCell biologyskeletogenesissea urchin developmentbiology.animalembryonic structuresGeneticsImmunohistochemistryp38 MAPK; SB203580; sea urchin development; skeletogenesisGeneral Agricultural and Biological SciencesSea urchin
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Oleuropein protects against dextran sodium sulfate-induced chronic colitis in mice.

2013

The anti-inflammatory effect of oleuropein (1), the major phenolic secoiridoid in Olea europaea, was evaluated in an experimental model of chronic colitis in mice. Animals were exposed to four repeated cycles of dextran sodium sulfate in drinking water followed by a 7-day rest period. Animals receiving a standard diet supplemented with 0.25% of 1 (equivalent to 500 mg/kg/day) for 56 days exhibited a decrease of inflammatory symptoms, as reflected by improvement of disease activity index and histopathological changes. It was found that 1 decreased inflammatory cell recruitment and the release of inflammatory cytokines interleukin (IL)-1β and IL-6 with increased IL-10 levels in colon tissue. …

T-LymphocytesInterleukin-1betaIridoid GlucosidesAnti-Inflammatory AgentsPharmaceutical ScienceNitric Oxide Synthase Type IIPharmacologyp38 Mitogen-Activated Protein KinasesAnalytical Chemistrychemistry.chemical_compoundMiceOleuropeinOleaDrug DiscoveryAnimalsIridoidsIntestinal MucosaChronic colitisPyransPharmacologybiologyMolecular StructureExperimental modelInterleukin-6Organic ChemistryDextran Sulfatebiology.organism_classificationColitisInterleukin-10Mice Inbred C57BLComplementary and alternative medicinechemistryOleaCyclooxygenase 2Molecular MedicineDextran sodium sulfateJournal of natural products
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Hematopoietic stem cell quiescence and function are controlled by the CYLD–TRAF2–p38MAPK pathway

2015

Tesio at al. identify a novel pathway controlled by the tumor suppressor and deubiquitinase cylindromatosis (CYLD), which is involved in the regulation of hematopoietic stem cell quiescence and repopulation potential.

TRAF2Tumor suppressor geneMAP Kinase Signaling SystemImmunologyRegulatorBiologyp38 Mitogen-Activated Protein KinasesArticleMicemedicineAnimalsImmunology and AllergyMice KnockoutRegulation of gene expressionNF-kappa BHematopoietic stem cellCell BiologyHematopoietic Stem CellsTNF Receptor-Associated Factor 2PhenotypeDeubiquitinating Enzyme CYLDCell biologyCysteine EndopeptidasesHaematopoiesismedicine.anatomical_structureGene Expression RegulationMutationStem cellJournal of Experimental Medicine
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Enzymatically hydrolyzed low-density lipoprotein modulates inflammatory responses in endothelial cells

2009

SummaryThere is evidence that low-density lipoprotein (LDL) is modified by hydrolytic enzymes,and that the product (E-LDL) induces selective production of interleukin 8 (IL-8) in endothelial cells. Since nuclear factor-kappaB (NF-κB) is a major regulator of IL-8 transcription, we studied its activation in endothelial cells treated with E-LDL. Unexpectedly,the modified lipoprotein not only failed to activate NF-κB, but completely blocked its activation by tumour necrosis factor-alpha (TNF-α) in EA.hy926-cells, as assessed by electrophoretic mobility shift assays and immunofluorescence. Inhibition occurred upstream of NF-κB translocation, as inhibitor of NF-κB- (IκB)-phosphorylation was suppr…

Time FactorsProto-Oncogene Proteins c-junPyridinesmedicine.medical_treatmentFatty Acids NonesterifiedBiologyp38 Mitogen-Activated Protein KinasesCell Linechemistry.chemical_compoundNF-KappaB Inhibitor alphamedicineHumansTrypsinInterleukin 8PhosphorylationPromoter Regions GeneticProtein Kinase InhibitorsTranscription factorInflammationTumor Necrosis Factor-alphaActivator (genetics)HydrolysisInterleukin-8ImidazolesTranscription Factor RelAEndothelial CellsNF-κBHematologySterol EsteraseMolecular biologyLipoproteins LDLTranscription Factor AP-1Endothelial stem cellCytokineBiochemistrychemistryLow-density lipoproteinI-kappa B ProteinsLipoproteinThrombosis and Haemostasis
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Cadmium effects on p38/MAPK isoforms in MDA-MB231 breast cancer cells

2009

Emerging evidence seems to indicate that the heavy metal cadmium (Cd) is able to regulate gene expression, drastically affecting the pattern of transcriptional activity in normal and pathological eukaryotic cells, also affecting intracellular signalization events. Human p38 is a family of mitogen-activated protein kinases consisting of four isoforms (alpha, beta, gamma and delta) which mediate signal transduction cascades controlling several aspects of cell physiology. In this study we examined whether exposure of MDA-MB231 tumor cells from the human breast to Cd may exert some effect on p38 isoform expression and accumulation, as well as on p38 activation. Employing a combination of prolif…

Transcriptional ActivationGene isoformCadmium SB203580 p38 isoforms p38 activation Gene expressionCell SurvivalPyridinesp38 mitogen-activated protein kinasesBreast NeoplasmsBiologyp38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicGeneral Biochemistry Genetics and Molecular BiologyBiomaterialsStructure-Activity RelationshipGene expressionTumor Cells CulturedHumansSettore BIO/06 - Anatomia Comparata E CitologiaCell ProliferationRegulation of gene expressionDose-Response Relationship DrugKinaseImidazolesMetals and AlloysMolecular biologyCell biologyIsoenzymesCell cultureDrug Screening Assays AntitumorSignal transductionGeneral Agricultural and Biological SciencesIntracellularCadmiumBioMetals
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The Streptococcal Exotoxin Streptolysin O Activates Mast Cells To Produce Tumor Necrosis Factor Alpha by p38 Mitogen-Activated Protein Kinase- and Pr…

2003

ABSTRACTStreptolysin O (SLO), a major virulence factor of pyogenic streptococci, binds to cholesterol in the membranes of eukaryotic cells and oligomerizes to form large transmembrane pores. While high toxin doses are rapidly cytocidal, low doses are tolerated because a limited number of lesions can be resealed. Here, we report that at sublethal doses, SLO activates primary murine bone marrow-derived mast cells to degranulate and to rapidly induce or enhance the production of several cytokine mRNAs, including tumor necrosis factor alpha (TNF-α). Mast cell-derived TNF-α plays an important protective role in murine models of acute inflammation, and the production of this cytokine was analyzed…

Transcriptional ActivationImmunologyBiologyp38 Mitogen-Activated Protein KinasesMicrobiologyMiceBacterial ProteinsmedicineAnimalsASK1Mast CellsRNA MessengerProtein kinase AProtein Kinase CProtein kinase CMice Inbred BALB CDose-Response Relationship DrugTumor Necrosis Factor-alphaMast cellMolecular PathogenesisProtein kinase RMolecular biologyInterleukin 33Infectious Diseasesmedicine.anatomical_structureStreptolysinsParasitologyTumor necrosis factor alphaStreptolysinMitogen-Activated Protein KinasesInfection and Immunity
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