Search results for " EXPERIMENTAL"

showing 10 items of 3530 documents

The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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Peroxisome proliferator-activated receptor alpha deficiency impairs regulatory T cell functions: Possible application in the inhibition of melanoma t…

2016

International audience; Regulatory T (Treg) cells are important to induce and maintain immunological self-tolerance. Although the progress accomplished in understanding the functional mechanism of Treg cells, intracellular molecules that control the mechanisms of their suppressive capacity are still on investigation. The present study showed that peroxisome proliferator-activated receptor-alpha deficiency impaired the suppressive activity of Treg cells on CD4(+)CD25(-) and CD8(+) T cell proliferation. In Treg cells, PPARα gene deletion also induced a decrease of migratory abilities, and downregulated the expression of chemokine receptors (CCR-4, CCR-8 and CXCR-4) and p27(KIP1) mRNA. Treg ce…

0301 basic medicineMaleAdoptive cell transferMESH: Tumor BurdenB16 melanoma tumorMelanoma ExperimentalMESH: T-Lymphocyte SubsetsCD4(+)CD25(+) regulatory T cellsBiochemistryMESH: Mice KnockoutImmunotherapy AdoptiveT-Lymphocytes RegulatoryPPARαMESH : T-Lymphocytes RegulatoryCell MovementT-Lymphocyte SubsetsMESH: Reverse Transcriptase Polymerase Chain ReactionMESH : Cell ProliferationMESH : Cell MovementMESH: AnimalsIL-2 receptorMESH: PPAR alphaMESH: Cell MovementCells CulturedMice KnockoutMESH : Melanoma ExperimentalbiologyMESH : Tumor BurdenReverse Transcriptase Polymerase Chain ReactionMESH : Reverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsGeneral MedicineMESH: Gene Expression Regulation Neoplastic3. Good healthTumor BurdenMESH: Melanoma ExperimentalDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureMESH: Immunotherapy AdoptiveReceptors ChemokineMESH : DNA-Binding ProteinsMESH: Cells Culturedmedicine.medical_specialtyMESH : Receptors ChemokineMESH: Cell Line TumorRegulatory T cellMESH : Gene Expression Regulation NeoplasticT cellMESH : MaleMESH : PPAR alphachemical and pharmacologic phenomenaMESH : Mice Inbred C57BLMESH : Clonal Anergy03 medical and health sciencesMESH: Mice Inbred C57BLInternal medicineMESH: Cell ProliferationCell Line TumorMESH : Cells CulturedmedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPPAR alpha[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCell ProliferationClonal AnergyPerforinMESH : Cell Line TumorMESH: T-Lymphocytes RegulatoryMolecular biologyMESH: MaleMESH : T-Lymphocyte SubsetsGranzyme BMice Inbred C57BL030104 developmental biologyEndocrinologyPerforinMESH: Clonal Anergybiology.proteinMESH : Mice KnockoutMESH : AnimalsMESH: Receptors ChemokineCD8MESH: DNA-Binding ProteinsMESH : Immunotherapy Adoptive
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Retrospective study of small pet tumors treated with Artemisia annua and iron.

2019

Artemisinin from Artemisia annua L. and its derivatives are well‑known antimalarial drugs. In addition, in vitro studies, in vivo studies and clinical trials have demonstrated that these drugs exhibit anticancer activity in human patients with cancer. Therefore, the aim of the present study was to investigate whether a phytotherapeutic A. annua preparation exerts anticancer activity in veterinary tumors of small pets. Dogs and cats with spontaneous cancer (n=20) were treated with standard therapy plus a commercial A. annua preparation (Luparte®) and compared with a control group treated with standard therapy alone (n=11). Immunohistochemical analyses were performed with formalin‑fixed paraf…

0301 basic medicineMaleCancer Researchnatural productsIronArtemisia annuaTransferrin receptorApoptosisBiologyPharmacologyArtemisia annuaAsteraceaeCat Diseaseschemotherapy03 medical and health sciences0302 clinical medicineDogsIn vivomedicineTumor Cells CulturedAnimalsDog DiseasesArtemisininProspective cohort studyCell ProliferationRetrospective StudiesOncogenePlant ExtractsCancerphytotherapyprognostic factorsNeoplasms ExperimentalArticlesbiology.organism_classificationmedicine.diseaseMolecular medicine030104 developmental biologyOncologyartemisinin030220 oncology & carcinogenesisCatsFemalemedicine.drugInternational journal of oncology
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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Fast direct neuronal signaling via the IL-4 receptor as therapeutic target in neuroinflammation.

2018

Ongoing axonal degeneration is thought to underlie disability in chronic neuroinflammation, such as multiple sclerosis (MS), especially during its progressive phase. Upon inflammatory attack, axons undergo pathological swelling, which can be reversible. Because we had evidence for beneficial effects of T helper 2 lymphocytes in experimental neurotrauma and discovered interleukin-4 receptor (IL-4R) expressed on axons in MS lesions, we aimed at unraveling the effects of IL-4 on neuroinflammatory axon injury. We demonstrate that intrathecal IL-4 treatment during the chronic phase of several experimental autoimmune encephalomyelitis models reversed disease progression without affecting inflamma…

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEncephalomyelitisInflammation03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsHumansAxonReceptorNeuroinflammationAdministration IntranasalInflammationNeuronsbusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitisTranslation (biology)General Medicinemedicine.diseaseAxonsReceptors Interleukin-4030104 developmental biologymedicine.anatomical_structurenervous systemInterleukin-4medicine.symptombusinessNeuroscience030217 neurology & neurosurgeryLocomotionScience translational medicine
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Large-scale genome-wide analysis identifies genetic variants associated with cardiac structure and function

2017

BACKGROUND: Understanding the genetic architecture of cardiac structure and function may help to prevent and treat heart disease. This investigation sought to identify common genetic variations associated with inter-individual variability in cardiac structure and function. METHODS: A GWAS meta-analysis of echocardiographic traits was performed, including 46,533 individuals from 30 studies (EchoGen consortium). The analysis included 16 traits of left ventricular (LV) structure, and systolic and diastolic function. RESULTS: The discovery analysis included 21 cohorts for structural and systolic function traits (n = 32,212) and 17 cohorts for diastolic function traits (n = 21,852). Replication …

0301 basic medicineMaleGenome-wide association studyBLOOD-PRESSUREResearch & Experimental Medicine030204 cardiovascular system & hematologyCoronary artery diseasegenome-wide0302 clinical medicineEPIDEMIOLOGYMyocardial infarctionGeneticsRISK11 Medical And Health SciencesGeneral Medicine3. Good healthMedicine Research & Experimentalcardiovascular systemMedical geneticsCORONARY-ARTERY-DISEASEHEART-FAILUREFemaleLife Sciences & Biomedicinemedicine.medical_specialtyHeart DiseasesImmunologyQuantitative trait locusPolymorphism Single Nucleotide03 medical and health sciencesQuantitative Trait HeritableGenetic variationmedicineHumansMETAANALYSISScience & Technologybusiness.industryMyocardiumta3121medicine.diseaseGenetic architecture030104 developmental biologyMYOCARDIAL-INFARCTIONGenetic LociHeart failureREPLICATIONClinical MedicinebusinessREDUCED EJECTION FRACTIONSUPPRESSOR GENEGenome-Wide Association Study
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Repurposing of the Antiepileptic Drug Levetiracetam to Restrain Neuroendocrine Prostate Cancer and Inhibit Mast Cell Support to Adenocarcinoma

2021

A relevant fraction of castration-resistant prostate cancers (CRPC) evolve into fatal neuroendocrine (NEPC) tumors in resistance to androgen deprivation and/or inhibitors of androgen receptor pathway. Therefore, effective drugs against both CRPC and NEPC are needed. We have previously described a dual role of mast cells (MCs) in prostate cancer, being capable to promote adenocarcinoma but also to restrain NEPC. This finding suggests that a molecule targeting both MCs and NEPC cells could be effective against prostate cancer. Using an in silico drug repurposing approach, here we identify the antiepileptic drug levetiracetam as a potential candidate for this purpose. We found that the protein…

0301 basic medicineMaleLevetiracetammast cellsneuroendocrine differentiationNeuroendocrine differentiationCell DegranulationAndrogen deprivation therapyProstate cancer0302 clinical medicineTumor Cells CulturedImmunology and AllergySV2AOriginal ResearchMembrane Glycoproteinsdrug repurposingCell Differentiationprostate cancerGene Expression Regulation NeoplasticMatrix Metalloproteinase 9030220 oncology & carcinogenesisAdenocarcinomaAnticonvulsantsLevetiracetammedicine.druglcsh:Immunologic diseases. AllergyImmunologyAntineoplastic AgentsMice TransgenicNerve Tissue Proteins03 medical and health sciencesmedicineAnimalsHumanstumor microenvironmentmouse modelsHigh-grade prostatic intraepithelial neoplasiadrug repurposing; mast cells; mouse models; neuroendocrine differentiation; prostate cancer; tumor microenvironmentCell Proliferationbusiness.industryDrug RepositioningProstatic NeoplasmsNeoplasms Experimentalmedicine.diseaseCarcinoma Neuroendocrinedrug repurposing mast cells mouse models neuroendocrine differentiation prostate cancer tumor microenvironmentAndrogen receptorMice Inbred C57BL030104 developmental biologyCancer researchlcsh:RC581-607business
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Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy.

2019

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxi…

0301 basic medicineMaleMice 129 StrainTime FactorsHeart DiseasesNitric Oxide Synthase Type IIIPhysiology030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicineEnosPhysiology (medical)medicineCyclic AMPCyclic GMP-Dependent Protein KinasesAnimalsDoxorubicinMyocytes CardiacCalcium SignalingRats WistarProtein kinase BCyclic GMPCells CulturedSimendanCardioprotectionMice KnockoutCardiotoxicityAntibiotics AntineoplasticbiologyDose-Response Relationship DrugChemistryCalcium-Binding ProteinsMammary Neoplasms ExperimentalCardiovascular AgentsLevosimendanbiology.organism_classificationCyclic AMP-Dependent Protein KinasesMyocardial ContractionCardiotoxicityPhospholambanMice Inbred C57BL030104 developmental biologyDoxorubicinMilrinoneFemaleCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktmedicine.drugCardiovascular research
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Effects of an Antimutagenic 1,4-Dihydropyridine AV-153 on Expression of Nitric Oxide Synthases and DNA Repair-related Enzymes and Genes in Kidneys of…

2016

Development of complications of diabetes mellitus (DM), including diabetic nephropathy, is a complex multi-stage process, dependent on many factors including the modification of nitric oxide (NO) production and an impaired DNA repair. The goal of this work was to study in vivo effects of 1,4-dihydropyridine AV-153, known as antimutagen and DNA binder, on the expression of several genes and proteins involved in NO metabolism and DNA repair in the kidneys of rats with a streptozotocin (STZ)-induced model of DM. Transcription intensity was monitored by means of real-time RT-PCR and the expression of proteins by immunohistochemistry. Development of DM significantly induced PARP1 protein express…

0301 basic medicineMalemedicine.medical_specialtyDihydropyridinesDNA RepairNitric Oxide Synthase Type IIIDNA repairPoly (ADP-Ribose) Polymerase-1Gene ExpressionNitric Oxide Synthase Type II030204 cardiovascular system & hematologyToxicologyKidneyNiacinStreptozocinNitric oxideDiabetes Mellitus ExperimentalDiabetic nephropathyHistones03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEnosInternal medicineGene expressionmedicineAnimalsRNA MessengerRats WistarGenePharmacologybiologyReverse Transcriptase Polymerase Chain ReactionKidney metabolismAntimutagenic AgentsGeneral Medicinemedicine.diseaseStreptozotocinbiology.organism_classificationPhosphoproteinsMolecular biologyRats030104 developmental biologyEndocrinologychemistrymedicine.drugBasicclinical pharmacologytoxicology
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