Search results for "signal transduction."

showing 10 items of 1278 documents

Cryptochlorogenic acid attenuates LPS-induced inflammatory response and oxidative stress via upregulation of the Nrf2/HO-1 signaling pathway in RAW 2…

2019

Phenolic acids are found in natural plants, such as caffeic acid, rosmarinic acid, and chlorogenic acid. They have long been used as pharmacological actives, owing to their anti-inflammatory and antioxidant activities. Cryptochlorogenic acid (CCGA) is a special isomer of chlorogenic acid; the pharmacological effects and related molecular mechanisms of CCGA have been poorly reported. In the present study, the antioxidant and anti-inflammatory effects of CCGA in RAW 264.7 macrophages and the underlying mechanisms were investigated. The results revealed that CCGA dose-dependently inhibited LPS-induced production of NO, TNF-α, and IL-6 and blocked iNOS, COX-2, TNF-α, and IL-6 expressions. CCGA …

0301 basic medicineLipopolysaccharidesAntioxidantMAP Kinase Signaling SystemNF-E2-Related Factor 2medicine.medical_treatmentImmunologyAnti-Inflammatory AgentsIκB kinasemedicine.disease_causeAntioxidants03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinemedicineCaffeic acidImmunology and AllergyAnimalsPharmacologyInflammationRosmarinic acidMacrophagesNF-kappa BMembrane ProteinsNF-κBGlutathioneCell biologyI-kappa B KinaseOxidative Stress030104 developmental biologyRAW 264.7 Cellschemistry030220 oncology & carcinogenesisSignal transductionChlorogenic AcidInflammation MediatorsOxidative stressHeme Oxygenase-1Signal TransductionInternational immunopharmacology
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Macrophage-induced reactive oxygen species promote myometrial contraction and labor-associated mechanisms

2020

AbstractAt labor, the myometrium is infiltrated by a massive influx of macrophages that secrete high levels of pro-inflammatory cytokines inducing the expression of specific labor-associated markers. However, the interactions between myocytes and macrophages and the role of macrophages in the myometrium at labor remain to be elucidated. In this work, we studied the role of myometrium-infiltrated macrophages and their interaction with myocytes in lipopolysaccharide-induced preterm labor. A co-culture model of human primary myometrial cells and macrophages was developed and validated. Collagen lattices were used to evaluate myocyte contraction. Differentiation steps were assessed by (i) phall…

0301 basic medicineLipopolysaccharideslabormacrophage03 medical and health scienceschemistry.chemical_compoundTransactivationUterine Contraction0302 clinical medicineMyocyteHumansoxidative stress[SDV.BDD]Life Sciences [q-bio]/Development BiologyCells Culturedmyocytechemistry.chemical_classificationReactive oxygen speciescell culture030219 obstetrics & reproductive medicinebiologySuperoxideMacrophagesMyometriumGap junctionParturitionCell DifferentiationCell BiologyGeneral MedicineHydrogen PeroxidedifferentiationVinculinCoculture TechniquesCell biology030104 developmental biologyReproductive Medicinechemistrybiology.proteinMyometriumFemaleSignal transductionReactive Oxygen Species
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Beta3 adrenergic receptor stimulation in human macrophages inhibits NADPHoxidase activity and induces catalase expression via PPARγ activation

2017

IF 4.521; International audience; The beta3 adrenergic receptor (β3-AR) stimulation plays a protective role against preterm labor by blocking myometrial contraction, cytokine production, remodeling and apoptosis. We previously demonstrated that macrophage-induced ROS production in the myometrium was a key element leading to the induction of all these labor-associated features. We thus aimed to investigate if the β3-AR could be expressed in human macrophages and could trigger its protective role in the myometrium by directly inhibiting ROS production. Using lipopolysaccharide (LPS)-stimulated myometrial samples and cell co-culture experiments, we demonstrated that β3-AR stimulation inhibits …

0301 basic medicineLipopolysaccharidesmedicine.medical_specialtyLipopolysaccharidePPARγPreterm laborMacrophagemedicine.medical_treatmentPeroxisome proliferator-activated receptorStimulationApoptosisAntioxidants03 medical and health scienceschemistry.chemical_compoundTransactivation0302 clinical medicineInternal medicinemedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologychemistry.chemical_classificationNADPH oxidasebiologybeta3 adrenergic receptorMacrophagesMyometriumNADPH OxidasesROSCell BiologyCatalaseCoculture Techniques3. Good healthCell biologyPPAR gamma030104 developmental biologyEndocrinologyCytokinechemistryGene Expression RegulationReceptors Adrenergic beta-3biology.proteinMyometriumFemaleSignal transductionReactive Oxygen Species030217 neurology & neurosurgerySignal Transduction
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Elafibranor, an Agonist of the Peroxisome Proliferator-Activated Receptor-alpha and -delta, Induces Resolution of Nonalcoholic Steatohepatitis Withou…

2016

International audience; BACKGROUND & AIMS: Elafibranor is an agonist of the peroxisome proliferator-activated receptor-α and peroxisome proliferator-activated receptor-δ. Elafibranor improves insulin sensitivity, glucose homeostasis, and lipid metabolism and reduces inflammation. We assessed the safety and efficacy of elafibranor in an international, randomized, double-blind placebo-controlled trial of patients with nonalcoholic steatohepatitis (NASH).METHODS: Patients with NASH without cirrhosis were randomly assigned to groups given elafibranor 80 mg (n = 93), elafibranor 120 mg (n = 91), or placebo (n = 92) each day for 52 weeks at sites in Europe and the United States. Clinical and …

0301 basic medicineLiver CirrhosisMaleTime FactorsIntention to Treat Analysi[SDV]Life Sciences [q-bio]BiopsyPLACEBO-CONTROLLED TRIALTHERAPYGastroenterologySeverity of Illness IndexChalcone0302 clinical medicineChalconesNon-alcoholic Fatty Liver DiseaseGastrointestinal AgentNonalcoholic fatty liver diseasePropionateMedicine and Health SciencesOdds RatioMedicineGlucose homeostasisVITAMIN-Eeducation.field_of_studyGastrointestinal agentFatty liverRemission InductionGastroenterologyMiddle Aged3. Good healthIntention to Treat AnalysisPPARDEuropeTreatment OutcomeLiverACIDPIOGLITAZONE030211 gastroenterology & hepatologyFemalePPARAHumanSignal TransductionAdultCLINICAL-OUTCOMESmedicine.medical_specialtyLogistic ModelTime FactorLiver CirrhosiPopulationfatty liver; NAFLD; PPARA; PPARD; Adult; Biomarkers; Biopsy; Chalcones; Double-Blind Method; Europe; Female; Gastrointestinal Agents; Humans; Intention to Treat Analysis; Liver; Liver Cirrhosis; Logistic Models; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Odds Ratio; PPAR alpha; PPAR gamma; Propionates; Remission Induction; Severity of Illness Index; Signal Transduction; Time Factors; Treatment Outcome; United States; GastroenterologyPlacebo03 medical and health sciencesDouble-Blind MethodGastrointestinal AgentsInternal medicineNAFLDHumansPPAR alphaeducationFATTY LIVER-DISEASEfatty liverHepatologybusiness.industryBiomarkerAMERICAN ASSOCIATIONOdds ratiomedicine.diseaseConfidence intervalUnited StatesPPAR gammaRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]030104 developmental biologyEndocrinologyLogistic ModelsHuman medicinePropionatesbusinessBiomarkers
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A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer's Disease, Glioblastoma and Lung cancer.

2017

Epidemiological studies indicate that patients suffering from Alzheimer’s disease have a lower risk of developing lung cancer, and suggest a higher risk of developing glioblastoma. Here we explore the molecular scenarios that might underlie direct and inverse co-morbidities between these diseases. Transcriptomic meta-analyses reveal significant numbers of genes with inverse patterns of expression in Alzheimer’s disease and lung cancer, and with similar patterns of expression in Alzheimer’s disease and glioblastoma. These observations support the existence of molecular substrates that could at least partially account for these direct and inverse co-morbidity relationships. A functional analy…

0301 basic medicineLung NeoplasmsMolecular biology[SDV]Life Sciences [q-bio]Gene ExpressionDiseaseCàncer--Fisiologia patològicaComorbidityTranscriptomeMedicineDinàmica molecularMultidisciplinaryQLung Cancer:Enginyeria biomèdica [Àrees temàtiques de la UPC]R3. Good healthAlzheimer's disease (AD)MedicineDisease SusceptibilityAlzheimer's diseaseSignal transductionSignal TransductionCentral Nervous System (CNS)ScienceModels BiologicalArticle03 medical and health sciencesImmune systemcáncerAlzheimer DiseaseDementia[CHIM]Chemical SciencesHumansLung cancerbusiness.industryGenetic Variationmedicine.diseaseComorbidityCNS cancerAlzheimer Malaltia d'030104 developmental biologyGliobastomas (GBM)ImmunologyCancer researchDementiabusinessGlioblastomaReactive Oxygen SpeciesNon-small-cell lung cancerBiomarkers
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Homeobox NKX2-3 promotes marginal-zone lymphomagenesis by activating B-cell receptor signalling and shaping lymphocyte dynamics

2016

NKX2 homeobox family proteins have a role in cancer development. Here we show that NKX2-3 is overexpressed in tumour cells from a subset of patients with marginal-zone lymphomas, but not with other B-cell malignancies. While Nkx2-3-deficient mice exhibit the absence of marginal-zone B cells, transgenic mice with expression of NKX2-3 in B cells show marginal-zone expansion that leads to the development of tumours, faithfully recapitulating the principal clinical and biological features of human marginal-zone lymphomas. NKX2-3 induces B-cell receptor signalling by phosphorylating Lyn/Syk kinases, which in turn activate multiple integrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MadCAM-1) a…

0301 basic medicineLymphoid TissueScienceB-cell receptorReceptors Antigen B-CellGeneral Physics and AstronomySykKaplan-Meier EstimateBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyNKX2-303 medical and health sciencesChemokine receptorstomatognathic systemLYNhemic and lymphatic diseasesmedicineAnimalsHumansSyk KinaseLymphocytesPhosphorylationB cellHomeodomain ProteinsMice KnockoutCàncer -- Aspectes molecularsMultidisciplinaryCell adhesion moleculeKinaseGene Expression ProfilingQLymphoma B-Cell Marginal ZoneGeneral Chemistryrespiratory system3. Good healthMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureembryonic structurescardiovascular systemCancer researchCell Adhesion MoleculesProteïnesSignal TransductionTranscription FactorsNature Communications
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Cannabinoid Control of Learning and Memory through HCN Channels

2016

The mechanisms underlying the effects of cannabinoids on cognitive processes are not understood. Here we show that cannabinoid type-1 receptors (CB1Rs) control hippocampal synaptic plasticity and spatial memory through the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels that underlie the h-current (Ih), a key regulator of dendritic excitability. The CB1R-HCN pathway, involving c-Jun-N-terminal kinases (JNKs), nitric oxide synthase, and intracellular cGMP, exerts a tonic enhancement of Ih selectively in pyramidal cells located in the superficial portion of the CA1 pyramidal cell layer, whereas it is absent from deep-layer cells. Activation of the CB1R-HCN pathway impairs d…

0301 basic medicineMAP Kinase Kinase 4medicine.medical_treatmentMorpholinesNeuroscience(all)RegulatorMice TransgenicBiologyNaphthalenesHippocampusBiophysical PhenomenaArticleMembrane Potentials03 medical and health sciencesMice0302 clinical medicineReceptor Cannabinoid CB1medicineHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsAnimalsEnzyme InhibitorsReceptorCyclic GMPSpatial MemoryMembrane potentialNeuronsGeneral NeuroscienceLong-term potentiationDendritesSynaptic PotentialsCalcium Channel BlockersBenzoxazines030104 developmental biologyMutationExcitatory postsynaptic potentialCannabinoidSignal transductionNitric Oxide SynthaseNeuroscience030217 neurology & neurosurgeryIntracellularSignal TransductionNeuron
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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Uncovering the Signaling Pathway behind Extracellular Guanine-Induced Activation of NO System: New Perspectives in Memory-Related Disorders

2018

Mounting evidence suggests that the guanine-based purines stand out as key player in cell metabolism and in several models of neurodegenerative disorders, such as Parkinson's and Alzheimer's diseases. Guanosine (GUO) and guanine (GUA) are extracellular signaling molecules derived from the breakdown of the correspondent nucleotide, GTP, and their intracellular and extracellular levels are regulated by the fine-tuned activity of two major enzymes, purine nucleoside phosphorylase (PNP) and guanine deaminase (GDA). Noteworthy, GUO and GUA, seem to play opposite roles in the modulation of cognitive functions, such as learning and memory. Indeed GUO, despite exerting neuroprotective, anti-apoptot…

0301 basic medicineMAPK/ERK pathwayCell signalingGuanineGuanosine03 medical and health scienceschemistry.chemical_compoundGuanine deaminase0302 clinical medicineCGMP; ERK; Guanine; L-NAME; Nitric oxide; SH-SY5Y cell line; Pharmacology; Pharmacology (medical)L-NAMEnitric oxideExtracellularguaninePharmacology (medical)Original ResearchPharmacologyChemistrylcsh:RM1-950Cell biologycGMPERKlcsh:Therapeutics. Pharmacology030104 developmental biologySignal transductionSH-SY5Y cell line030217 neurology & neurosurgeryIntracellularFrontiers in Pharmacology
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Therapeutic resistance in breast cancer cells can result from deregulated EGFR signaling

2020

The epidermal growth factor receptor (EGFR) interacts with various downstream molecules including phospholipase C (PLC)/protein kinase C (PKC), Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/GSK-3, Jak/STAT and others. Often these pathways are deregulated in human malignancies such as breast cancer. Various therapeutic approaches to inhibit the activity of EGFR family members including small molecule inhibitors and monoclonal antibodies (MoAb) have been developed. A common problem with cancer treatments is the development of drug-resistance. We examined the effects of a conditionally-activated EGFR (v-Erb-B:ER) on the resistance of breast cancer cells to commonly used chemotherapeutic drugs such as doxorub…

0301 basic medicineMAPK/ERK pathwayEGFRvIIICancer ResearchEGFREstrogen receptorAntineoplastic AgentsBreast Neoplasms03 medical and health sciences0302 clinical medicineBreast cancerBreast cancerCell Line TumorGeneticsHumansMedicinePTENEpidermal growth factor receptorskin and connective tissue diseasesMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologybusiness.industryCancermedicine.diseaseErbB Receptors030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisDrug resistancebiology.proteinCancer researchMolecular MedicineFemalebusinessSignal TransductionV-Erb-B
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