Search results for "arginine"

showing 10 items of 389 documents

Cationic Amino Acid Transporter-1-Mediated Arginine Uptake Is Essential for Chronic Lymphocytic Leukemia Cell Proliferation and Viability

2019

Interfering with tumor metabolism by specifically restricting the availability of extracellular nutrients is a rapidly emerging field of cancer research. A variety of tumor entities depend on the uptake of the amino acid arginine since they have lost the ability to synthesize it endogenously, that is they do not express the rate limiting enzyme for arginine synthesis, argininosuccinate synthase (ASS). Arginine transport through the plasma membrane of mammalian cells is mediated by eight different transporters that belong to two solute carrier (SLC) families. In the present study we found that the proliferation of primary as well as immortalized chronic lymphocytic leukemia (CLL) cells depen…

0301 basic medicineCancer ResearchArginineArgininosuccinate synthaseargininelcsh:RC254-282amino acid transporter03 medical and health sciences0302 clinical medicineDownregulation and upregulationhemic and lymphatic diseasesAmino acid transporterViability assayOriginal Researchchemistry.chemical_classificationnutrient restrictionArginine transportbiologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAmino acidSolute carrier familyCell biology030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisbiology.proteinchronic lymphocytic leukemiatumor metabolismFrontiers in Oncology
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Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis

2016

Ductal occlusion has been postulated to precipitate focal pancreatic inflammation, while the nature of the primary occluding agents has remained elusive. Neutrophils make use of histone citrullination by peptidyl arginine deiminase-4 (PADI4) in contact to particulate agents to extrude decondensed chromatin as neutrophil extracellular traps (NETs). In high cellular density, NETs form macroscopically visible aggregates. Here we show that such aggregates form inside pancreatic ducts in humans and mice occluding pancreatic ducts and thereby driving pancreatic inflammation. Experimental models indicate that PADI4 is critical for intraductal aggregate formation and that PADI4-deficiency abrogates…

0301 basic medicineExtracellular TrapsHydrolasesNeutrophilsScienceGeneral Physics and AstronomyBiologyExtracellular TrapsArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciencesPancreatic JuiceProtein-Arginine Deiminase Type 4medicineAnimalsHumansPancreasCeruletideMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionQInterleukin-17Pancreatic DuctsGeneral ChemistryNeutrophil extracellular trapsFlow Cytometrymedicine.diseaseImmunohistochemistryChromatinCell biologyChromatinDisease Models AnimalHistone citrullination030104 developmental biologymedicine.anatomical_structurePancreatitisChronic DiseasePancreatic juiceImmunologyProtein-Arginine DeiminasesCytokinesPancreatitisPancreasCeruletideNature Communications
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Venlafaxine prevents morphine antinociceptive tolerance: The role of neuroinflammation and the l-arginine-nitric oxide pathway.

2017

Abstract Opioid-induced neuroinflammation and the nitric oxide (NO) signal-transduction pathway are involved in the development of opioid analgesic tolerance. The antidepressant venlafaxine (VLF) modulates NO in nervous tissues, and so we investigated its effect on induced tolerance to morphine, neuroinflammation, and oxidative stress in mice. Tolerance to the analgesic effects of morphine were induced by injecting mice with morphine (50 mg/kg) once a day for three consecutive days; the effect of co-administration of VLF (5 or 40 mg/kg) with morphine was similarly tested in a separate group. To determine if the NO precursor l -arginine hydrochloride ( l -arg) or NO are involved in the effec…

0301 basic medicineMaleArginineAnalgesicPharmacologymedicine.disease_causeNitric oxideProinflammatory cytokine03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDevelopmental NeurosciencemedicineAnimalsEnzyme InhibitorsNitritesPain Measurementchemistry.chemical_classificationGlutathione PeroxidaseDose-Response Relationship DrugMorphineGlutathione peroxidaseVenlafaxine HydrochlorideBrainMalondialdehydeAnalgesics OpioidDisease Models AnimalOxidative Stress030104 developmental biologyNG-Nitroarginine Methyl EsterNeurologychemistryMorphineAntidepressive Agents Second-GenerationCytokinesLipid PeroxidationMorphine Dependence030217 neurology & neurosurgeryOxidative stressmedicine.drugSignal TransductionExperimental neurology
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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Relation between high levels of myeloperoxidase in the culprit artery and microvascular obstruction, infarct size and reverse remodeling in ST-elevat…

2017

International audience; MAIN OBJECTIVE: To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI).METHOD: 40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences.RESULTS: Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO g…

0301 basic medicineMalePhysiologyNeutrophilsMyocardial Infarctionlcsh:Medicine030204 cardiovascular system & hematologyBiochemistryVentricular Function Leftchemistry.chemical_compoundWhite Blood CellsOxidative Damage0302 clinical medicineAnimal CellsMedicine and Health SciencesDiseaseMyocardial infarction[ SDV.IB ] Life Sciences [q-bio]/Bioengineeringlcsh:ScienceMultidisciplinaryEjection fractionbiologyVentricular RemodelingNeurochemistryStroke volumeArteriesMiddle Aged[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemPathophysiologyBody FluidsBloodMyeloperoxidaseCreatinineCardiologyFemale[SDV.IB]Life Sciences [q-bio]/BioengineeringAnatomyNeurochemicalsCellular TypesResearch Articlemedicine.medical_specialtyImmune CellsImmunologyCardiologyMagnetic Resonance Imaging CineNitric OxideLong-TermBlood PlasmaNo-Reflow03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicineDimethylargininemedicineHumanscardiovascular diseasesMortalityVentricular remodelingAgedPeroxidaseCreatinineBlood Cellsbusiness.industryMicrocirculationlcsh:RBiology and Life SciencesStroke VolumeCell BiologyDefinitionLeukocytemedicine.diseaseTroponin030104 developmental biologychemistrybiology.proteinCardiovascular AnatomyBlood VesselsST Elevation Myocardial Infarctionlcsh:QbusinessReactive Oxygen SpeciesAcute Coronary SyndromesBiomarkersNeuroscienceEjection Fraction
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Increased Symmetric Dimethylarginine Level Is Associated with Worse Hospital Outcomes through Altered Left Ventricular Ejection Fraction in Patients …

2017

International audience; Objectives: We aimed to investigate whether SDMA-symmetric dimethylarginine-the symmetrical stereoisomer of ADMA-might be a marker of left ventricular function in AMI.Background: Asymmetric dimethylarginine (ADMA) has been implicated in the prognosis after acute myocardial infarction (AMI) and heart failure (HF).Methods: Cross sectional prospective study from 487 consecutive patients hospitalized 2, and death.Results: Patients were analysed based on SDMA tertiles. Sex, diabetes, dyslipidemia, and prior MI were similar for all tertiles. In contrast, age and hypertension increased across the tertiles (p<0.001). From the first to the last tertile, GRACE risk score was e…

0301 basic medicineMalePhysiologyPerformanceMyocardial Infarctionlcsh:MedicineBlood PressureChronic Heart-Failure030204 cardiovascular system & hematologyVascular MedicineBiochemistryVentricular Function Leftchemistry.chemical_compound0302 clinical medicineChronic Kidney DiseaseMedicine and Health SciencesCoronary Heart DiseaseDiseaseMyocardial infarctionProspective cohort studylcsh:ScienceMultidisciplinaryFramingham Risk ScoreEjection fractionAsymmetric DimethylarginineNeurochemistryMiddle AgedMetaanalysis[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemPrognosisArteryHospitals3. Good healthTreatment OutcomeImpactNephrologyHypertensionCardiologyFemaleAnatomyNeurochemicalsResearch ArticleGlomerular Filtration Ratemedicine.medical_specialtyCardiologyRenal functionNitric OxideArginine03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineHumansRenal Insufficiency ChronicMortalityAgedHeart FailureRenal Physiologybusiness.industrylcsh:RBiology and Life SciencesRenal SystemMarkermedicine.diseaseRenal-Function030104 developmental biologychemistryHeart failurelcsh:QAsymmetric dimethylargininebusinessDyslipidemiaNeuroscience
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Antibody-mediated blockade of JMJD6 interaction with collagen I exerts antifibrotic and antimetastatic activities

2017

JMJD6 is known to localize in the nucleus, exerting histone arginine demethylase and lysyl hydroxylase activities. A novel localization of JMJD6 in the extracellular matrix, resulting from its secretion as a soluble protein, was unveiled by a new anti-JMJD6 mAb called P4E11, which was developed to identify new targets in the stroma. Recombinant JMJD6 binds with collagen type I (Coll-I), and distinct JMJD6 peptides interfere with collagen fibrillogenesis, collagen-fibronectin interaction, and adhesion of human tumor cells to the collagen substrate. P4E11 and collagen binding to JMJD6 are mutually exclusive because the amino acid sequences of JMJD6 necessary for the interaction with Coll-I ar…

0301 basic medicineMonoclonal antibodyXenograft Model Antitumor AssayArginineLysyl hydroxylaseEnzyme-Linked Immunosorbent AssayReceptors Cell SurfacePlasma protein bindingBiochemistryCollagen Type IExtracellular matrix03 medical and health sciencesMiceFibrosisPeptide LibraryCell Line TumormedicineGeneticsAnimalsHumansOsteonectinCell NucleuMolecular BiologyCell NucleusMice KnockoutMice Inbred BALB CbiologyChemistryJmjC familyAnimalAntibodies MonoclonalFibrillogenesisExtracellular matrixmedicine.diseaseXenograft Model Antitumor AssaysImmunohistochemistryCell biologyIn vivo treatment030104 developmental biologybiology.proteinOsteonectinSignal transductionExtracellular matrix; In vivo treatment; JmjC family; Monoclonal antibody; Peptide library; Animals; Antibodies Monoclonal; Cell Line Tumor; Cell Nucleus; Collagen Type I; Enzyme-Linked Immunosorbent Assay; Extracellular Matrix; Humans; Immunohistochemistry; Mice; Mice Inbred BALB C; Mice Knockout; Osteonectin; Peptide Library; Protein Binding; Receptors Cell Surface; Signal Transduction; Xenograft Model Antitumor Assays; Biotechnology; Biochemistry; Molecular Biology; GeneticsHumanProtein BindingSignal TransductionBiotechnology
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Neutrophil extracellular traps impair fungal clearance in a mouse model of invasive pulmonary aspergillosis

2019

Abstract Neutrophil extracellular traps (NETs) are formed by polymorphonuclear neutrophils (PMN) and contribute to the innate host defense by binding and killing bacterial and fungal pathogens. Because NET formation depends on histone hypercitrullination by peptidylarginine deiminase 4 (PAD4), we used PAD4 gene deficient (Pad4-/-) mice in a mouse model of invasive pulmonary aspergillosis (IPA) to address the contribution of NETs to the innate host defense in vivo. After the induction (24 h) of IPA by i.t. infection with Aspergillus fumigatus conidia, Pad4-/- mice revealed lower fungal burden in the lungs, accompanied by less acute lung injury, TNFα and citH3 compared to wildtype controls. T…

0301 basic medicineNeutrophilsImmunologyMedizinApoptosisLung injuryExtracellular TrapsArticleAspergillus fumigatusMicrobiologyMice03 medical and health sciences0302 clinical medicineProtein-Arginine Deiminase Type 4In vivomedicineAnimalsHumansImmunology and Allergyskin and connective tissue diseasesLungInvasive Pulmonary AspergillosisMice KnockoutLungbiologyAspergillus fumigatusWild typeHematologyNeutrophil extracellular trapsbiology.organism_classificationmedicine.diseaseImmunity Innaterespiratory tract diseasesMice Inbred C57BLDisease Models AnimalPneumonia030104 developmental biologymedicine.anatomical_structureCitrullinationTumor necrosis factor alpha030215 immunologyImmunobiology
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PIWIL3 Forms a Complex with TDRKH in Mammalian Oocytes.

2019

P-element induced wimpy testis (PIWIs) are crucial guardians of genome integrity, particularly in germ cells. While mammalian PIWIs have been primarily studied in mouse and rat, a homologue for the human PIWIL3 gene is absent in the Muridae family, and hence the unique function of PIWIL3 in germ cells cannot be effectively modeled by mouse knockouts. Herein, we investigated the expression, distribution, and interaction of PIWIL3 in bovine oocytes. We localized PIWIL3 to mitochondria, and demonstrated that PIWIL3 expression is stringently controlled both spatially and temporally before and after fertilization. Moreover, we identified PIWIL3 in a mitochondrial-recruited three-membered complex…

0301 basic medicineTransposable elementendocrine systemCytoplasmArgininetransposonMutagenesis (molecular biology technique)Piwi-interacting RNAEmbryonic DevelopmentmammalpiRNABiologyMitochondrionArginineArticle03 medical and health sciences0302 clinical medicinemedicineAnimalsAmino Acid SequenceRNA Small Interferingoocytelcsh:QH301-705.5GeneGene knockoutMuridaegenomic integrityPIWIRNA-Binding ProteinsGeneral Medicinebiology.organism_classificationOocyteCell biologyMitochondriaProtein Transport030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)Argonaute ProteinsExoribonucleasesDNA Transposable ElementsOocytesCattle030217 neurology & neurosurgeryFunction (biology)Protein BindingCells
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Surge of Peripheral Arginine Vasopressin in a Rat Model of Birth Asphyxia

2018

Mammalian birth is accompanied by a period of obligatory asphyxia, which consists of hypoxia (drop in blood O2 levels) and hypercapnia (elevation of blood CO2 levels). Prolonged, complicated birth can extend the asphyxic period, leading to a pathophysiological situation, and in humans, to the diagnosis of clinical birth asphyxia, the main cause of hypoxic-ischemic encephalopathy (HIE). The neuroendocrine component of birth asphyxia, in particular the increase in circulating levels of arginine vasopressin (AVP), has been extensively studied in humans. Here we show for the first time that normal rat birth is also accompanied by an AVP surge, and that the fetal AVP surge is further enhanced in…

0301 basic medicineVasopressinmedicine.medical_specialtySTRESSArgininehypothalamic-pituitary axis (HPA axis)blood gasesHYPOXIAbirth asphyxia3124 Neurology and psychiatrylcsh:RC321-571neonatal03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineCopeptinInternal medicineMedicineBRAINlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPRECURSORNEURONSperinatalOriginal ResearchRELEASEAsphyxiaFetusPARAVENTRICULAR NUCLEUSbusiness.industry3112 NeurosciencescopeptinENCEPHALOPATHYarginine vasopressin (AVP)Hypoxia (medical)base deficit030104 developmental biologyEndocrinologyHypothalamusHYPOTHALAMUSmedicine.symptombusinessHypercapnia030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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