Search results for "signal transduction."

showing 10 items of 1278 documents

Exercise and Metformin Intervention Prevents Lipotoxicity-Induced Hepatocyte Apoptosis by Alleviating Oxidative and ER Stress and Activating the AMPK…

2022

Objective. Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2DM) commonly coexist and act synergistically to drive adverse clinical outcomes. This study is aimed at investigating the effects of exercise intervention and oral hypoglycaemic drug of metformin (MET) alone or combined on hepatic lipid accumulation. To investigate if oxidative stress and endoplasmic reticulum stress (ERS) are involved in lipotoxicity-induced hepatocyte apoptosis in diabetic mice and whether exercise and/or MET alleviated oxidative stress or ERS-apoptosis by AMPK-Nrf2-HO-1 signaling pathway. Methods. Forty db/db mice with diabetes ( random   blood   glucose ≥ 250   mg / dL ) were randomly allocated i…

Blood GlucoseAgingArticle SubjectNF-E2-Related Factor 2metformiiniApoptosisAMP-Activated Protein KinasesBiochemistryAntioxidantsDiabetes Mellitus ExperimentalMiceohjelmoitunut solukuolemaSuperoxide Dismutase-1aineenvaihduntahäiriötAnimalsHypoglycemic AgentsHematoxylinoksidatiivinen stressibcl-2-Associated X ProteinCaspase 3Cell BiologyGeneral MedicineEndoplasmic Reticulum StressLipidsMetforminOxidative StressDiabetes Mellitus Type 2ei-alkoholiperäinen rasvamaksasairausHepatocyteslääkehoitoEosine Yellowish-(YS)koe-eläinmallitaikuistyypin diabetesSignal TransductionliikuntahoitoOxidative Medicine and Cellular Longevity
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Does Glycemic Control Modulate the Impairment of NLRP3 Inflammasome Activation in Type 2 Diabetes?

2019

Since mitochondrial dysfunction is associated with NOD-like receptor family protein 3 (NLRP3) activation in type 2 diabetes (T2D), which can eventually lead to an impaired immune response, we set out to determine if glycemic control modulates the effects of T2D on the NLRP3 inflammasome. We have studied leukocytes from 61 diabetic patients [25 with glycated hemoglobin (HbA(1c)) 7% and 36 with HbA(1c) 8%] and 40 healthy controls. Total and mitochondrial reactive oxygen species (ROS) production was enhanced in T2D patients, and mitochondrial ROS was more pronounced in those with poor glycemic control. Levels of gene and protein expression of NLRP3 were decreased in both diabetic groups and mo…

Blood GlucoseMale0301 basic medicineMitochondrial ROSendocrine system diseasesInflammasomesPhysiologyClinical BiochemistryType 2 diabetesmedicine.disease_causeBiochemistrychemistry.chemical_compoundGene expressionoxidative stressGeneral Environmental Scienceintegumentary systemInterleukinInflammasomeMiddle AgedMitochondriaglycaemic controlCytokinesFemaletype 2 diabetesInflammation MediatorsSignal Transductionmedicine.drugmedicine.medical_specialty03 medical and health sciencesmitochondrial functionInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineHumansBody Weights and MeasuresMolecular BiologyAgedGlycemicGlycated Hemoglobin030102 biochemistry & molecular biologybusiness.industrynutritional and metabolic diseasesCell Biologymedicine.diseaseNLRP3 inflammasome030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2chemistryGeneral Earth and Planetary SciencesGlycated hemoglobinReactive Oxygen SpeciesbusinessBiomarkersOxidative stressAntioxidants & Redox Signaling
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Hypothalamic Apelin/Reactive Oxygen Species Signaling Controls Hepatic Glucose Metabolism in the Onset of Diabetes

2014

Aims: We have previously demonstrated that central apelin is implicated in the control of peripheral glycemia, and its action depends on nutritional (fast versus fed) and physiological (normal versus diabetic) states. An intracerebroventricular (icv) injection of a high dose of apelin, similar to that observed in obese/diabetic mice, increase fasted glycemia, suggesting (i) that apelin contributes to the establishment of a diabetic state, and (ii) the existence of a hypothalamic to liver axis. Using pharmacological, genetic, and nutritional approaches, we aim at unraveling this system of regulation by identifying the hypothalamic molecular actors that trigger the apelin effect on liver gluc…

Blood GlucoseMaleSympathetic nervous systemLIVER[SDV.BIO]Life Sciences [q-bio]/BiotechnologyGlycogenolysisPhysiology[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionClinical BiochemistryMice ObeseBiochemistrySYMPATHETIC-NERVE ACTIVITYAPELINBRAINGeneral Environmental ScienceINSULIN-RESISTANCE3. Good healthApelinOriginal Research CommunicationsADIPOSE-TISSUEmedicine.anatomical_structureIntercellular Signaling Peptides and ProteinsSignal TransductionEXPRESSIONmedicine.medical_specialtyGlycogenolysisHypothalamusBiologyCarbohydrate metabolismAutonomic Nervous SystemInsulin resistanceAdipokinesInternal medicineDiabetes mellitusmedicineAnimalsMolecular BiologyGluconeogenesis[ SDV.BIO ] Life Sciences [q-bio]/BiotechnologyCell Biologymedicine.diseaseMice Inbred C57BLMICEGlucoseEndocrinologyDiabetes Mellitus Type 2GluconeogenesisRATGeneral Earth and Planetary SciencesLiver functionReactive Oxygen Species[SDV.AEN]Life Sciences [q-bio]/Food and NutritionSYSTEMAntioxidants & Redox Signaling
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The sodium-glucose co-transporter 2 inhibitor empagliflozin improves diabetes-induced vascular dysfunction in the streptozotocin diabetes rat model b…

2014

Objective In diabetes, vascular dysfunction is characterized by impaired endothelial function due to increased oxidative stress. Empagliflozin, as a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), offers a novel approach for the treatment of type 2 diabetes by enhancing urinary glucose excretion. The aim of the present study was to test whether treatment with empagliflozin improves endothelial dysfunction in type I diabetic rats via reduction of glucotoxicity and associated vascular oxidative stress. Methods Type I diabetes in Wistar rats was induced by an intravenous injection of streptozotocin (60 mg/kg). One week after injection empagliflozin (10 and 30 mg/kg/d) was adminis…

Blood GlucoseMalemedicine.medical_treatmentReceptor for Advanced Glycation End Productslcsh:MedicineGene ExpressionType 2 diabetesmedicine.disease_causeVascular MedicineGlucosidesMedicine and Health SciencesMedicineInsulinEndothelial dysfunctionReceptors Immunologiclcsh:ScienceMultidisciplinaryType 1 DiabetesCytokinesInflammation Mediatorsmedicine.drugSignal TransductionResearch Articlemedicine.medical_specialtyCardiologyBlood sugarStreptozocinCardiovascular PharmacologyDiabetes Mellitus ExperimentalDiabetes ComplicationsInternal medicineDiabetes mellitusEmpagliflozinDiabetes MellitusAnimalsRNA MessengerVascular DiseasesBenzhydryl CompoundsSodium-Glucose Transporter 2 InhibitorsPharmacologybusiness.industryInsulinlcsh:RHemodynamicsStreptozotocinmedicine.diseaseRatsOxidative StressEndocrinologyGlucoseMetabolic Disorderslcsh:QbusinessOxidative stressDiabetic AngiopathiesPloS one
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Hydroxychloroquine, COVID ‐19 and diabetes. Why it is a different story

2020

Hydroxychloroquine has been proposed for the cure of the COVID-19 due to its anti-inflammatory and anti-viral action. People with diabetes are more prone to severe outcome if affected by COVID-19 and the use of Hydroxychloroquine might have some benefit in this setting. However, the use of Hydroxychloroquine in diabetes deserves particular attention for its documented hypoglycemic action.

Blood Glucosemedicine.medical_specialty2019-20 coronavirus outbreakCoronavirus disease 2019 (COVID-19)Endocrinology Diabetes and MetabolismSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)MEDLINE030209 endocrinology & metabolismGlycemic Control030204 cardiovascular system & hematologySeverity of Illness IndexDiabetes Complications03 medical and health sciences0302 clinical medicineEndocrinologyCommentariesInternal medicineDiabetes mellitusSeverity of illnessDiabetes MellitusInternal MedicinemedicineHyperglycaemiaHumansHypoglycemic AgentsBlood Glucose COVID-19 Diabetes Complications Diabetes Mellitus Glycemic Control Humans Hydroxychloroquine Hypoglycemic Agents SARS-CoV-2 Severity of Illness Index Signal TransductionSARS-CoV-2business.industryDiabetesCOVID-19Hydroxychloroquinemedicine.diseaseCOVID-19 Drug TreatmentACE2 Cardiovascular disease COVID‐19CommentarybusinessHydroxychloroquineSignal Transductionmedicine.drugDiabetes/Metabolism Research and Reviews
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The Inflammatory Role of Platelets : Translational Insights from Experimental Studies of Autoimmune Disorders

2016

Beyond their indispensable role in hemostasis, platelets have shown to affect the development of inflammatory disorders, as they have been epidemiologically and mechanistically linked to diseases featuring an inflammatory reaction in inflammatory diseases like multiple sclerosis, rheumatoid arthritis and inflammatory bowel disorders. The identification of novel molecular mechanisms linking inflammation and to platelets has highlighted them as new targets for therapeutic interventions. In particular, genetic and pharmacological studies have identified an important role for platelets in neuroinflammation. This review summarizes the main molecular links between platelets and inflammation, focu…

Blood Platelets0301 basic medicineMultiple SclerosisMedizinInflammationReviewmedicine.disease_causeCatalysisAutoimmune DiseasesneuroinflammationAutoimmunityArthritis Rheumatoidlcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineImmune systemAnimalsHumansMedicinePlateletPhysical and Theoretical ChemistryReceptorlcsh:QH301-705.5Molecular BiologySpectroscopyNeuroinflammationInflammationbusiness.industryMultiple sclerosisautoimmunityOrganic ChemistryGeneral MedicineInflammatory Bowel Diseasesmedicine.diseaseComputer Science Applications030104 developmental biologylcsh:Biology (General)lcsh:QD1-999030220 oncology & carcinogenesisplateletsImmunologymedicine.symptomSignal transductionbusiness
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The Gut Microbiota as an Influencing Factor of Arterial Thrombosis

2018

The mutualistic gut microbiota does not only impact the development and function of various immune cell types, but it also influences the function of the hepatic vascular endothelium and prothrombotic platelet function. With germ-free mouse models, we have demonstrated that gut-derived microbial-associated molecular patterns could stimulate hepatic von Willebrand factor (VWF) synthesis and plasmatic VWF levels through Toll-like receptor-2 (TLR2), thus defining the extent of platelet deposition to the subendothelial matrix of the ligation-injured common carotid artery. In addition to the microbiota-derived choline metabolite trimethylamine N-oxide and the microbiota's regulatory role on the …

Blood Platelets030204 cardiovascular system & hematologyGut floradigestive system03 medical and health sciences0302 clinical medicineImmune systemVon Willebrand factorAnimalsHumansPlateletInnate immune systembiologyEndothelial CellsThrombosisArteriesHematologybiology.organism_classificationGastrointestinal MicrobiomeTLR2CoagulationImmunologybiology.proteinSignal transductionSignal Transduction030215 immunologyHämostaseologie
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Dual role of the p38 MAPK/cPLA2 pathway in the regulation of platelet apoptosis induced by ABT-737 and strong platelet agonists.

2013

p38 Mitogen-activated protein (MAP) kinase is involved in the apoptosis of nucleated cells. Although platelets are anucleated cells, apoptotic proteins have been shown to regulate platelet lifespan. However, the involvement of p38 MAP kinase in platelet apoptosis is not yet clearly defined. Therefore, we investigated the role of p38 MAP kinase in apoptosis induced by a mimetic of BH3-only proteins, ABT-737, and in apoptosis-like events induced by such strong platelet agonists as thrombin in combination with convulxin (Thr/Cvx), both of which result in p38 MAP kinase phosphorylation and activation. A p38 inhibitor (SB202190) inhibited the apoptotic events induced by ABT-737 but did not influ…

Blood PlateletsCancer ResearchcPLA2p38 mitogen-activated protein kinasesImmunologyBlotting Westernp38 Mitogen-Activated Protein KinasesPiperazinesNitrophenolsCellular and Molecular NeurosciencePhospholipase A2Crotalid VenomsHumansLectins C-Typeddc:610Cells CulturedMembrane Potential MitochondrialplateletSulfonamidesbiologyKinaseGroup IV Phospholipases A2Biphenyl CompoundsapoptosisConvulxinCell BiologyFlow Cytometryp38 MAP kinaseCell biologyApoptosisMitogen-activated protein kinasebiology.proteinPhosphorylationOriginal ArticleSignal transductionReactive Oxygen SpeciesSignal TransductionCell deathdisease
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Differential roles of cAMP and cGMP in megakaryocyte maturation and platelet biogenesis

2012

The cyclic nucleotides cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) regulate the activity of protein kinase A (PKA) and protein kinase G (PKG), respectively. This process helps maintain circulating platelets in a resting state. Here we studied the role of cAMP and cGMP in the regulation of megakaryocyte (MK) differentiation and platelet formation. Cultured, platelet-producing MKs were differentiated from fetal livers harvested from 13.5 days postcoital mouse embryos. MK development was accompanied by a dramatic increase in cAMP production and expression of soluble guanylate cyclase, PKG, and PKA as well as their downstream targets vasodilator-stimulated ph…

Blood PlateletsCancer Researchmegakaryocytes; cAMP; cGMP; plateletsPhosphodiesterase 3BiologyArticleAdenylyl cyclaseMicechemistry.chemical_compoundPregnancyCyclic AMPGeneticsAnimalsCyclic adenosine monophosphatePhosphorylationProtein kinase ACyclic GMPMolecular BiologyCyclic guanosine monophosphateMicrofilament ProteinsCell DifferentiationCell BiologyHematologyPhosphoproteinsCyclic AMP-Dependent Protein KinasesCell biologyMice Inbred C57BLCytoskeletal ProteinsThrombopoietinchemistrycAMP-dependent pathwayFemalePDE10ASignal transductionCell Adhesion MoleculesMegakaryocytesExperimental Hematology
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Time-resolved characterization of cAMP/PKA-dependent signaling reveals that platelet inhibition is a concerted process involving multiple signaling p…

2014

One of the most important physiological platelet inhibitors is endothelium-derived prostacyclin which stimulates the platelet cyclic adenosine monophosphate/protein kinase A (cAMP/PKA)-signaling cascade and inhibits virtually all platelet-activating key mechanisms. Using quantitative mass spectrometry, we analyzed time-resolved phosphorylation patterns in human platelets after treatment with iloprost, a stable prostacyclin analog, for 0, 10, 30, and 60 seconds to characterize key mediators of platelet inhibition and activation in 3 independent biological replicates. We quantified over 2700 different phosphorylated peptides of which 360 were significantly regulated upon stimulation. This com…

Blood PlateletsImmunologyProstacyclinBiologyBiochemistrychemistry.chemical_compoundCyclic AMPmedicineHumansCyclic adenosine monophosphateIloprostProtein Interaction MapsPlatelet activationPhosphorylationProtein kinase AKinaseCell BiologyHematologyPlatelet ActivationCyclic AMP-Dependent Protein KinaseschemistryBiochemistryPlatelet aggregation inhibitorPhosphorylationSignal transductionPlatelet Aggregation InhibitorsSignal Transductionmedicine.drugBlood
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