Search results for "messenger"

showing 10 items of 1493 documents

Anti-diabetic effects of mildronate alone or in combination with metformin in obese Zucker rats

2010

Abstract Mildronate is a cardioprotective drug, the mechanism of action of which is based on the regulation of l -carnitine concentration. We studied the metabolic effects of treatment with mildronate, metformin and a combination of the two in the Zucker rat model of obesity and impaired glucose tolerance. Zucker rats were p.o. treated daily with mildronate (200 mg/kg), metformin (300 mg/kg), and a combination of both drugs for 4 weeks. Weight gain and plasma metabolites reflecting glucose metabolism were measured. The expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ and target genes was measured in rat heart and liver tissues. Each treatment decreased the blood …

Blood GlucoseMalemedicine.medical_specialtymedicine.medical_treatmentPeroxisome proliferator-activated receptorCarbohydrate metabolismImpaired glucose toleranceEatingInternal medicinemedicineAnimalsHypoglycemic AgentsInsulinPPAR alphaLactic AcidObesityRNA MessengerCarnitineCell NucleusPharmacologychemistry.chemical_classificationbusiness.industryMyocardiumInsulinBody WeightLipid Metabolismmedicine.diseaseMetforminRatsRats ZuckerMetforminPPAR gammaDrug CombinationsEndocrinologyGene Expression RegulationMechanism of actionchemistryCarnitine biosynthesismedicine.symptombusinessMethylhydrazinesmedicine.drugEuropean Journal of Pharmacology
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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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Peroxisome Proliferator-Activated Receptor Deficiency Increases the Risk of Maternal Abortion and Neonatal Mortality in Murine Pregnancy with or with…

2006

We assessed the implication of peroxisome proliferator-activated receptor (PPAR) alpha deficiency in pregnancy outcome and neonatal survival and in the modulation of T cell differentiation in murine diabetic pregnancy and their offspring. Pregnant wild-type (WT) and PPAR alpha-null mice of C57BL/6J genetic background were rendered diabetic by five low doses of streptozotocin. We observed that, in the absence of diabetes, PPAR alpha deficiency resulted in an increase in abortion rate, i.e. 0% in WT mice vs. 20% in PPAR alpha-null mice [odds ratio (OR) = 14.33; P = 0.013]. Under diabetic conditions, the abortion rate was enhanced, i.e. 8.3% in WT mice vs. 50% in PPAR alpha-null mice (OR = 4.2…

Blood Glucosemedicine.medical_specialtyOffspringRatónT-LymphocytesPeroxisome proliferator-activated receptorBiologyPeroxisomeDiabetes Mellitus ExperimentalInterferon-gammaMiceEndocrinologyTh2 CellsDownregulation and upregulationPregnancyDiabetes mellitusInternal medicinemedicineAnimalsInsulinPPAR alphaLymphocyte CountRNA MessengerReceptorFetal Deathchemistry.chemical_classificationMice KnockoutPregnancy[SCCO.NEUR]Cognitive science/NeuroscienceCell DifferentiationTh1 CellsStreptozotocinmedicine.diseaseLipidsInterleukin-10Abortion SpontaneousMice Inbred C57BLPregnancy ComplicationsEndocrinologychemistry[ SCCO.NEUR ] Cognitive science/NeuroscienceCytokinesInterleukin-2FemaleInterleukin-4Spleenmedicine.drug
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Correction of glycaemia and GLUT1 level by mildronate in rat streptozotocin diabetes mellitus model

2011

Anti-ischaemic drug mildronate suppresses fatty acid metabolism and increases glucose utilization in myocardium. It was proposed that it could produce a favourable effect on metabolic parameters and glucose transport in diabetic animals. Rats with streptozotocin diabetes mellitus were treated with mildronate (100 mg/kg daily, per os, 6 weeks). Therapeutic effect of mildronate was monitored by measuring animal weight, concentrations of blood glucose, insulin, blood triglycerides, free fatty acids, blood ketone bodies and cholesterol, glycated haemoglobin per cent (HbA1c%) and glucose tolerance. GLUT1 mRNA and protein expression in kidneys, heart, liver and muscles were studied by means of re…

Blood Glucosemedicine.medical_specialtyendocrine system diseasesmedicine.medical_treatmentClinical BiochemistryBiochemistryStreptozocinDiabetes Mellitus Experimentalchemistry.chemical_compoundInternal medicineDiabetes mellitusDiabetes MellitusmedicineAnimalsBody SizeHypoglycemic AgentsInsulinRNA MessengerRats WistarTriglyceridesGlycated HemoglobinGlucose Transporter Type 1Glucose tolerance testmedicine.diagnostic_testFatty acid metabolismbiologyCholesterolbusiness.industryInsulinFatty AcidsGlucose transporternutritional and metabolic diseasesCell BiologyGeneral MedicineGlucose Tolerance Testmedicine.diseaseRatsEndocrinologychemistrybiology.proteinKetone bodiesGLUT1businessMethylhydrazinesCell Biochemistry and Function
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Change in Protein Phenotype without a Nucleus: Translational Control in Platelets

2004

For most cells the nucleus takes center stage. Not only is it the largest organelle in eukaryotic cells, it carries most of the genome and transcription of DNA to RNA largely takes place in the nucleus. Because transcription is a major step in gene regulation, the absence of a nucleus is limiting from a biosynthetic standpoint. Consequently, the anucleate status of platelets has stereotyped it as a cell without synthetic potential. It is now clear, however, that this viewpoint is far too simplistic. In response to physiologic stimuli, platelets synthesize biologically relevant proteins that are regulated via gene expression programs at the translational level. This process does not require …

Blood PlateletsCell NucleusRegulation of gene expressionGeneticsMessenger RNATranscription GeneticCellBlood ProteinsHematologyBiologyGenetic translationCell biologyPhenotypemedicine.anatomical_structureTranscription (biology)Protein BiosynthesisGene expressionmedicineAnimalsHumansRNA MessengerThrombopoiesisCardiology and Cardiovascular MedicineRibosomesNucleusSeminars in Thrombosis and Hemostasis
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The histone deacetylase sirtuin 2 is a new player in the regulation of platelet function

2015

SummaryBackground Histone deacetylases (HDACs) play a key role in signaling in many cell types. However, little is known about the participation of HDACs, particularly sirtuins (SIRTs), in platelet reactivity. Objective To investigate the role of HDACs in platelets, we examined the effects of SIRT inhibition on platelet function and protein acetylation in human platelets. Methods We used washed platelets obtained from healthy subjects. Cambinol (SIRT1 and SIRT2 inhibitor), AGK2 (specific SIRT2 inhibitor) and EX527 (specific SIRT1 inhibitor) were used as SIRT inhibitors. Platelets were stimulated with collagen, thrombin, or U46619, and platelet responses were determined according to optical …

Blood PlateletsPlatelet AggregationCytoplasmic GranulesSIRT2Glycogen Synthase Kinase 3Akt3 protein kinaseSirtuin 2sirtuinsHumansPlateletRNA MessengerPhosphorylationProtein kinase Bacetylationblood plateletGlycogen Synthase Kinase 3 betabiologySecretory VesiclesAcetylationHematologyCell biologyHistone Deacetylase InhibitorsBiochemistryAcetylationSirtuinbiology.proteinPhosphorylationPlatelet aggregation inhibitorCalciumHistone deacetylaseProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktPlatelet Aggregation Inhibitorssignal transductionSignal TransductionJournal of Thrombosis and Haemostasis
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Differential Expression Analysis by RNA-Seq Reveals Perturbations in the Platelet mRNA Transcriptome Triggered by Pathogen Reduction Systems

2015

Platelet concentrates (PCs) are prepared at blood banks for transfusion to patients in certain clinical conditions associated with a low platelet count. To prevent transfusion-transmitted infections via PCs, different pathogen reduction (PR) systems have been developed that inactivate the nucleic acids of contaminating pathogens by chemical cross-linking, a mechanism that may also affect platelets' nucleic acids. We previously reported that treatment of stored platelets with the PR system Intercept significantly reduced the level of half of the microRNAs that were monitored, induced platelet activation and compromised the platelet response to physiological agonists. Using genome-wide differ…

Blood Plateletslcsh:MedicinePlatelet Transfusion030204 cardiovascular system & hematologyBiologyTranscriptome03 medical and health sciences0302 clinical medicineNucleic AcidsGene expressionmicroRNAHumansPlateletRNA MessengerPlatelet activationlcsh:Science030304 developmental biologyMedicinsk genetik0303 health sciencesMultidisciplinarySequence Analysis RNAlcsh:RKlinisk medicinRNAPlatelet ActivationMolecular biology3. Good healthMicroRNAsPlatelet transfusionBlood PreservationNucleic acidBlood Bankslcsh:QClinical MedicineTranscriptomeMedical GeneticsResearch Article
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The down-regulation of miR-125b in chronic lymphocytic leukemias leads to metabolic adaptation of cells to a transformed state

2012

AbstractMiR-125b-1 maps at 11q24, a chromosomal region close to the epicenter of 11q23 deletions in chronic lymphocytic leukemias (CLLs). Our results establish that both aggressive and indolent CLL patients show reduced expression of miR-125b. Overexpression of miR-125b in CLL-derived cell lines resulted in the repression of many transcripts encoding enzymes implicated in cell metabolism. Metabolomics analyses showed that miR-125b overexpression modulated glucose, glutathione, lipid, and glycerolipid metabolism. Changes on the same metabolic pathways also were observed in CLLs. We furthermore analyzed the expression of some of miR-125b–target transcripts that are potentially involved in the…

Blotting WesternImmunologyBiologyReal-Time Polymerase Chain ReactionBiochemistryNODownregulation and upregulationmicroRNABiomarkers TumorHumansMetabolomicsRNA MessengerPsychological repressionCells CulturedCell ProliferationOligonucleotide Array Sequence AnalysisRegulation of gene expressionB-LymphocytesLymphoid NeoplasiaReverse Transcriptase Polymerase Chain ReactionCell growthGene Expression ProfilingCell BiologyHematologyLeukemia Lymphocytic Chronic B-CellMolecular biologyGene Expression Regulation NeoplasticGene expression profilingMicroRNAsMetabolic pathwayCell Transformation NeoplasticChromosomal regionCancer researchBlood
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Altered expression of nonclassical HLA class Ib antigens in human renal cell carcinoma and its association with impaired immune response

2003

Abstract An optimal antitumoral immune response requires the activation of both CD8 + and CD4 + T lymphocytes by the peptide antigen presentation via the human leukocyte antigen (HLA) class I and class II molecules, respectively. Downregulation or loss of HLA molecules has been found in human renal cell carcinoma (RCC) and provides a strategy of these tumors to evade T-cell mediated immunosurveillance. In addition, a tumor-specific upregulation of HLA-G has been recently described in RCC, which also leads to an impaired immune response. We here summarize the frequency of the constitutive and/or interferon-γ (IFN-γ) inducible expression of nonclassical HLA class Ib antigens in RCC cell lines…

Blotting WesternImmunologyHuman leukocyte antigenBiologyurologic and male genital diseasesInterferon-gammaImmune systemAntigenDownregulation and upregulationHLA AntigensInterferonTumor Cells CulturedmedicineHumansImmunology and AllergyRNA MessengerCarcinoma Renal CellHLA-G AntigensKidneyReverse Transcriptase Polymerase Chain ReactionHistocompatibility Antigens Class IAntibodies MonoclonalGeneral MedicineFlow CytometryKidney NeoplasmsRecombinant ProteinsUp-RegulationGene Expression Regulation NeoplasticKiller Cells NaturalImmunosurveillanceBlotting Southernmedicine.anatomical_structureImmunologyCD8T-Lymphocytes Cytotoxicmedicine.drugHuman Immunology
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Overexpression of bone morphogenetic protein-6 (BMP-6) in the epidermis of transgenic mice: inhibition or stimulation of proliferation depending on t…

1996

Bone morphogenetic protein-6 (BMP-6) belongs to the family of TGF-beta-related growth factors. In the developing epidermis, expression of BMP-6 coincides with the onset of stratification. Expression persists perinatally but declines after day 6 postpartum, although it can still be detected in adult skin by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. We constitutively overexpressed BMP-6 in suprabasal layers of interfollicular epidermis in transgenic mice using a keratin 10 promoter. All mice expressing the transgene developed abnormalities in the skin, indicating an active transgene-derived factor. Depending on the pattern of transgene expression, the effects on proli…

Bone Morphogenetic Protein 6Cellular differentiationTransgenemedicine.medical_treatmentMice TransgenicHuman skinIntegrin alpha6BiologyBone morphogenetic proteinMiceDermisAntigens CDmedicineAnimalsHumansPsoriasisAcanthosis NigricansRNA MessengerPromoter Regions GeneticSkinEpidermis (botany)Growth factorStomachMouth MucosaGene Expression Regulation DevelopmentalCell DifferentiationKeratosisArticlesCell BiologyKeratin-10Cell biologyBone morphogenetic protein 6medicine.anatomical_structureAnimals NewbornEpidermal CellsBone Morphogenetic ProteinsImmunologyKeratinsEpidermisCell DivisionJournal of Cell Biology
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