Search results for "SIGNALLING"

showing 10 items of 249 documents

NUPR1 protects liver from lipotoxic injury by improving the endoplasmic reticulum stress response

2021

AbstractBackground and AimsNon-alcoholic fatty liver disease and related hepatic syndromes affect up to one third of the adult population. The molecular mechanisms underlying NAFL etiology remain elusive. Nuclear Protein 1 (NUPR1) expression increases upon cell injury in all organs and recently we report its active participation in the activation of the Unfolded Protein Response (UPR). The UPR typically maintains protein homeostasis, but downstream mediators of the pathway regulate metabolic functions, including lipid metabolism. NUPR1 and UPR increase have been reported in obesity and liver pathologies and the goal of this study was to investigate the roles of NUPR1 in this context.Methods…

0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaPPAR-a signalling UPRPeroxisome proliferator-activated receptorContext (language use)UPRDiet High-FatBiochemistry03 medical and health sciencesLiver diseaseMice0302 clinical medicineInternal medicineCell Line TumorGeneticsmedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationbusiness.industryEndoplasmic reticulumFatty liverNASHLipid metabolismlipotoxicitymedicine.diseaseEndoplasmic Reticulum StressLipid MetabolismNeoplasm Proteins030104 developmental biologyEndocrinologychemistryLipotoxicityLiverNAFLKnockout mouseUnfolded protein responseUnfolded Protein ResponsePPAR-a signallingSteatosisSteatohepatitisbusiness030217 neurology & neurosurgeryNUPR1Biotechnology
researchProduct

Resveratrol Interferes with IL1-β-Induced Pro-Inflammatory Paracrine Interaction between Primary Chondrocytes and Macrophages

2016

International audience; State of the art. Osteoarthritis (OA) is a chronic articular disease characterized by cartilage degradation and osteophyte formation. OA physiopathology is multifactorial and involves mechanical and hereditary factors. So far, there is neither preventive medicine to delay cartilage breakdown nor curative treatment. Objectives. To investigate pro-inflammatory paracrine interactions between human primary chondrocytes and macrophages following interleukin-1-β (IL-1β) treatment; to evaluate the molecular mechanism responsible for the inhibitory effect of resveratrol. Results. The activation of NF-κB in chondrocytes by IL-1β induced IL-6 secretion. The latter will then ac…

0301 basic medicinemedicine.medical_specialtyTime Factors[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionInterleukin-1betalcsh:TX341-641InflammationmacrophageResveratrolresveratrolChondrocyteArticleNF-κBSTAT303 medical and health scienceschemistry.chemical_compoundParacrine signallingChondrocytesInternal medicineStilbenesmedicineMacrophageHumansSecretionCells CulturedInflammationNutrition and DieteticsCartilageMacrophagesAnti-Inflammatory Agents Non-SteroidalNF-κBIL1-β; chondrocyte; macrophage; NF-κB; STAT3; resveratrolCoculture TechniquesCell biology030104 developmental biologyEndocrinologymedicine.anatomical_structurechemistrychondrocytemedicine.symptomIL1-βlcsh:Nutrition. Foods and food supplyBiomarkersFood ScienceNutrients
researchProduct

Conditioned Medium from Human Amnion-Derived Mesenchymal Stromal/Stem Cells Attenuating the Effects of Cold Ischemia-Reperfusion Injury in an In Vitr…

2021

The clinical results of lung transplantation (LTx) are still less favorable than other solid organ transplants in both the early and long term. The fragility of the lungs limits the procurement rate and can favor the occurrence of ischemia-reperfusion injury (IRI). Ex vivo lung perfusion (EVLP) with Steen SolutionTM (SS) aims to address problems, and the implementation of EVLP to alleviate the activation of IRI-mediated processes has been achieved using mesenchymal stromal/stem cell (MSC)-based treatments. In this study, we investigated the paracrine effects of human amnion-derived MSCs (hAMSCs) in an in vitro model of lung IRI that includes cold ischemia and normothermic EVLP. We found tha…

0301 basic medicinemedicine.medical_treatmentApoptosislcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5Cells CulturedSpectroscopyamnion-derived mesenchymal stem cellsCell CycleCold IschemiaNF-kappa BCell DifferentiationGeneral MedicineComputer Science Applicationsconditioned mediummedicine.anatomical_structureReperfusion Injury030220 oncology & carcinogenesisCytokinesStem cellStromal cellCell Survivalex vivo lung perfusionArticleCatalysisInorganic Chemistry03 medical and health sciencesParacrine signallingDownregulation and upregulationmedicineHumansLung transplantationAmnionlung ischemia-reperfusion injuryPhysical and Theoretical ChemistryMolecular BiologyLungbusiness.industryOrganic ChemistryMesenchymal stem cellMesenchymal Stem Cellsmedicine.disease030104 developmental biologyGene Expression Regulationlcsh:Biology (General)lcsh:QD1-999A549 CellsAlveolar Epithelial CellsCulture Media ConditionedCancer researchbusinessReperfusion injuryInternational Journal of Molecular Sciences
researchProduct

Proteomics Reveals the Potential Protective Mechanism of Hydrogen Sulfide on Retinal Ganglion Cells in an Ischemia/Reperfusion Injury Animal Model

2020

Glaucoma is the leading cause of irreversible blindness and is characterized by progressive retinal ganglion cell (RGC) degeneration. Hydrogen sulfide (H2S) is a potent neurotransmitter and has been proven to protect RGCs against glaucomatous injury in vitro and in vivo. This study is to provide an overall insight of H2S&rsquo

0301 basic medicineneuronal apoptosisgenetic structuresQuantitative proteomicshydrogen sulfidePharmaceutical Sciencelcsh:Medicinelcsh:RS1-441PharmacologyProteomicsRetinal ganglionArticlelabel-free mass spectrometrylcsh:Pharmacy and materia medica03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemitochondrial functionIn vivoDrug DiscoverymedicineRetinaChemistrylcsh:RRetinalmedicine.diseaseequipment and supplieseye diseases030104 developmental biologymedicine.anatomical_structureglaucomaRetinal ganglion cellMolecular Medicinesense organsReperfusion injurysignalling pathways030217 neurology & neurosurgeryPharmaceuticals
researchProduct

CD73-generated extracellular adenosine in chronic lymphocytic leukemia creates local conditions counteracting drug-induced cell death

2011

Abstract Extracellular adenosine (ADO), generated from ATP or ADP through the concerted action of the ectoenzymes CD39 and CD73, elicits autocrine and paracrine effects mediated by type 1 purinergic receptors. We have tested whether the expression of CD39 and CD73 by chronic lymphocytic leukemia (CLL) cells activates an adenosinergic axis affecting growth and survival. By immunohistochemistry, CD39 is widely expressed in CLL lymph nodes, whereas CD73 is restricted to proliferation centers. CD73 expression is highest on Ki-67+ CLL cells, adjacent to T lymphocytes, and is further localized to perivascular areas. CD39+/CD73+ CLL cells generate ADO from ADP in a time- and concentration-dependen…

AdenosineCellular differentiationChronic lymphocytic leukemia5'-Nucleotidase; Adenosine; Adenosine Diphosphate; Adenosine Triphosphate; Antigens CD; Antineoplastic Agents Phytogenic; Apyrase; Autocrine Communication; Cell Death; Cell Differentiation; Cell Movement; Cell Survival; Etoposide; Extracellular Space; GPI-Linked Proteins; Humans; Leukemia Lymphocytic Chronic B-Cell; Paracrine Communication; Receptor Adenosine A2A; Tumor Cells Cultured; Biochemistry; Immunology; Hematology; Cell BiologyMICROENVIRONMENTCD38BiochemistryACTIVATIONAdenosine TriphosphateCell MovementPhytogenichemic and lymphatic diseasesTumor Cells CulturedChronic5'-NucleotidaseEtoposideLeukemiaCulturedCell DeathTUMOR-GROWTHApyrasePurinergic receptorCell DifferentiationHematologyLymphocyticCDTumor CellsCell biologyAdenosine DiphosphateAutocrine CommunicationLeukemiaReceptorIMMUNE SUPPRESSIONReceptor Adenosine A2ACell SurvivalImmunologyAntineoplastic AgentsAdenosinergicBiologyGPI-Linked ProteinsDAMAGE-INDUCED APOPTOSISAdenosine A2AParacrine signallingAntigens CDParacrine CommunicationmedicineHumansAntigensAutocrine signallingImmunobiologyB-CellCell BiologyDAMAGE-INDUCED APOPTOSIS; T-CELLS; IMMUNE SUPPRESSION; ZAP-70 EXPRESSION; TUMOR-GROWTH; RECEPTOR; CD73; ACTIVATION; CD38; MICROENVIRONMENTmedicine.diseaseAntineoplastic Agents PhytogenicLeukemia Lymphocytic Chronic B-CellSettore MED/15 - MALATTIE DEL SANGUET-CELLSCD73Extracellular SpaceZAP-70 EXPRESSIONCD38Blood
researchProduct

CD4+ CCR5+ and CD4+ CCR3+ lymphocyte subset and monocyte apoptosis in patients with acute visceral leishmaniasis

2004

The potential involvement of apoptosis in the pathogenesis of visceral leishmaniasis (VL) was examined by studying spontaneous and Leishmania antigen (LAg)-induced apoptosis using cryopreserved peripheral blood mononuclear cells (PBMC) of Sicilian patients with VL. Results indicate that monocytes and T lymphocytes from acute VL patients show a significantly higher level of apoptosis compared with that observed in healed subjects. The percentage of apoptotic cells was higher in monocytes than in T lymphocytes. T cells involved in programmed cell death (PCD) were mainly of the CD4(+) phenotype. In particular, the T helper 1-type (Th1) subset, as evaluated by chemokine receptor-5 (CCR5) expres…

AdultCD4-Positive T-LymphocytesProgrammed cell deathChemokineReceptors CCR5Receptors CCR3ImmunologyAntigens ProtozoanApoptosisCD8-Positive T-LymphocytesBiologyPeripheral blood mononuclear cellMonocytesParacrine signallingAntigenmedicineHumansImmunology and Allergyfas ReceptorAutocrine signallingCells CulturedMonocyteOriginal ArticlesTh1 CellsLymphocyte Subsetsmedicine.anatomical_structureApoptosisAcute DiseaseImmunologyLeukocytes Mononuclearbiology.proteinLeishmaniasis VisceralReceptors ChemokineImmunology
researchProduct

The leptin system during human endometrial receptivity and preimplantation development.

2004

The leptin system is implicated in the regulation of body weight and reproductive function, acting at endocrine and paracrine levels. This ligand-receptor system is mandatory for embryonic implantation in rodents. Here, we investigate the expression pattern of total leptin receptor (OB-R(T)), the long form (OB-R(L)) and short isoforms HuB219.1 and HuB219.3 in the human endometrium. Furthermore, we studied leptin and OB-R(T) mRNA during human embryonic preimplantation development and the embryonic regulation of the endometrial OB-R(L). Leptin receptor expression and its isoforms increase in the luteal phase and peak in the late part. Leptin receptor was localized at the epithelial and glandu…

AdultLeptinmedicine.medical_specialtyEndocrinology Diabetes and MetabolismClinical BiochemistryReceptors Cell SurfaceBiologyEndometriumBiochemistryPolymerase Chain ReactionParacrine signallingEmbryonic and Fetal DevelopmentEndometriumEndocrinologyInternal medicinemedicineHumansProtein IsoformsBlastocystEmbryo ImplantationRNA MessengerMenstrual CycleCytotrophoblastLeptin receptorReverse Transcriptase Polymerase Chain ReactionLeptindigestive oral and skin physiologyBiochemistry (medical)DeciduaEmbryogenesisImmunohistochemistrymedicine.anatomical_structureEndocrinologyBlastocystReceptors LeptinFemalehormones hormone substitutes and hormone antagonistsThe Journal of clinical endocrinology and metabolism
researchProduct

Apoptosis resistance in epithelial tumors is mediated by tumor-cell-derived interleukin-4

2008

We investigated the mechanisms involved in the resistance to cell death observed in epithelial cancers. Here, we identify that primary epithelial cancer cells from colon, breast and lung carcinomas express high levels of the antiapoptotic proteins PED, cFLIP, Bcl-xL and Bcl-2. These cancer cells produced interleukin-4 (IL-4), which amplified the expression levels of these antiapoptotic proteins and prevented cell death induced upon exposure to TRAIL or other drug agents. IL-4 blockade resulted in a significant decrease in the growth rate of epithelial cancer cells and sensitized them, both in vitro and in vivo, to apoptosis induction by TRAIL and chemotherapy via downregulation of the antia…

AdultMaleProgrammed cell deathLung NeoplasmsTime Factorsapoptosis interleukin-4 cancer stem cells cancer chemiotherapy cytokinesCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsBiologyTNF-Related Apoptosis-Inducing LigandTumor Cells CulturedmedicineHumansAutocrine signallingMolecular BiologyInterleukin 4AgedCell ProliferationSettore MED/04 - Patologia GeneraleCell DeathDose-Response Relationship DrugCell growthCarcinomaIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalInterleukin-4 Receptor alpha SubunitCorrectionCancerCell BiologyMiddle AgedPhosphoproteinsmedicine.diseaseUp-RegulationCell biologyAutocrine CommunicationProto-Oncogene Proteins c-bcl-2Drug Resistance NeoplasmApoptosisColonic NeoplasmsCancer cellFemaleInterleukin-4Interleukin-4 Cancer stem cellsSignal transductionApoptosis Regulatory ProteinsSignal Transduction
researchProduct

Low-intensity exercise stimulates bioenergetics and increases fat oxidation in mitochondria of blood mononuclear cells from sedentary adults.

2020

Aim Exercise training induces adaptations in muscle and other tissue mitochondrial metabolism, dynamics, and oxidative phosphorylation capacity. Mitochondrial fatty acid oxidation was shown to be pivotal for the anti‐inflammatory status of immune cells. We hypothesize that exercise training can exert effects influence mitochondrial fatty acid metabolism in peripheral blood mononuclear cells (PBMCs). The aim was to investigate the effect of exercise on the fatty acid oxidation‐dependent respiration in PBMCs. Design Twelve fasted or fed volunteers first performed incremental‐load exercise tests to exhaustion on a cycle ergometer to determine the optimal workload ensuring maximal health benefi…

AdultMalemedicine.medical_specialtyobesityBioenergeticsPhysiologyImmunologyOxidative phosphorylation030204 cardiovascular system & hematologylcsh:Physiologyexercise fat metabolism lipolysis obesity sedentary adultsSignalling Pathways03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicineRespirationHeart ratemedicineMetabolism and RegulationLipolysisHumansBeta oxidationSedentary lifestyleOriginal Researchchemistry.chemical_classificationlcsh:QP1-981exercisebusiness.industryEndurance and PerformanceFatty Acidsfat metabolismFatty acidFastingsedentary adultsLipid MetabolismMitochondriaEndocrinologychemistryExercise TestLeukocytes MononuclearPhysical EndurancelipolysisFemaleSedentary BehaviorbusinessEnergy MetabolismOxidation-Reduction030217 neurology & neurosurgeryPhysiological reports
researchProduct

Definition of discrete signals involved in human T-cell activation

1986

Abstract Mitogenic activities of monoclonal antibodies directed at denned receptor structures expressed on the surface of mature human T lymphocytes were employed to study, in detail, signals involved in primary T-cell activation. Based on differential requirements for stimulation, two discrete pathways of human T-cell activation can be defined: the antigen-induced mode of activation initiated through the Ti-T3 antigen-receptor complex and an alternative pathway which can be triggered by monoclonal antibodies directed at the T11 glycoprotein. Perhaps more importantly, the approach taken here allows the definition of stable intermediate cellular stages within the activation cascade and, thus…

Adultmedicine.drug_classT-LymphocytesT cellImmunologyReceptors Antigen T-CellAntigen-Presenting CellsStimulationBiologyLymphocyte ActivationMonoclonal antibodyMonocytesmedicineHumansReceptorMolecular Biologychemistry.chemical_classificationAntibodies MonoclonalCell biologySignallingmedicine.anatomical_structurechemistryAlternative complement pathwayInterleukin-2GlycoproteinInterleukin-1Molecular Immunology
researchProduct