Search results for "C57BL"

showing 10 items of 1292 documents

Mas receptor is involved in the estrogen-receptor induced nitric oxide-dependent vasorelaxation.

2017

The Mas receptor is involved in the angiotensin (Ang)-(1-7) vasodilatory actions by increasing nitric oxide production (NO). We have previously demonstrated an increased production of Ang-(1-7) in human umbilical vein endothelial cells (HUVEC) exposed to estradiol (E2), suggesting a potential cross-talk between E2 and the Ang-(1-7)/Mas receptor axis. Here, we explored whether the vasoactive response and NO-related signalling exerted by E2 are influenced by Mas. HUVEC were exposed to 10nM E2 for 24h in the presence or absence of the selective Mas receptor antagonist A779, and the estrogen receptor (ER) antagonist ICI182780 (ICI). E2 increased Akt and endothelial nitric oxide synthase (eNOS) …

0301 basic medicineMalemedicine.medical_specialtyEstrogen receptorVasodilationNitric OxideBiochemistryProto-Oncogene MasUmbilical veinNitric oxideReceptors G-Protein-Coupled03 medical and health scienceschemistry.chemical_compoundMiceEnosInternal medicineProto-Oncogene ProteinsmedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansProtein kinase BPharmacologybiologyAntagonistbiology.organism_classificationMice Inbred C57BLVasodilation030104 developmental biologyEndocrinologychemistryReceptors EstrogenMyographBiochemical pharmacology
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A Network Involving Gut Microbiota, Circulating Bile Acids, and Hepatic Metabolism Genes That Protects Against Non-Alcoholic Fatty Liver Disease.

2019

Scope Gut microbiota contributes to non-alcoholic fatty liver disease (NAFLD) pathogenesis by multiple mechanisms not yet completely understood. Novel differential features between germ-free mice (GFm) transplanted with protective or non-protective cecal microbiota against NAFLD are investigated. Methods and results Gut microbiota composition, plasma, and fecal bile acids (BAs) and liver mRNAs are quantified in GFm recipients from four donor mice differing in NAFLD severity (control diet, high-fat diet [HFD]-responder, HFD-non-responder, and quercetin-supplemented HFD). Transplanted GFm are on control or HFD for 16-weeks. Multivariate analysis shows that GFm colonized with microbiota from H…

0301 basic medicineMalemedicine.medical_specialtyGut floraDiet High-Fatdigestive systemPathogenesisBile Acids and Salts03 medical and health sciencesMiceNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineAnimalsFeces030109 nutrition & dieteticsbiologyEthanoldigestive oral and skin physiologyFatty livernutritional and metabolic diseasesTransporterbiology.organism_classificationmedicine.diseasePhenotypeGastrointestinal MicrobiomeMice Inbred C57BL030104 developmental biologyEndocrinologyLiverBacteroidesTranscriptomeDrug metabolismFood ScienceBiotechnologyMolecular nutritionfood research
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Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain.

2018

Growing evidence suggests a link between obesity and neurodegeneration. The purpose of the present study was to explore the neuroprotective potential of glucagon-like peptide-2 (GLP-2) in the brain of high fat diet (HFD)-fed mice. Markers of inflammation and oxidative stress were analysed in the brains of obese mice chronically treated with [Gly2]-GLP-2 (teduglutide), the stable analogue of the GLP-2, and they were compared to age-matched untreated obese and lean animals. Neurodegeneration was examined by TUNEL assay. HFD feeding increased the expression of pro-inflammatory mediators (NF-kB, IL-8, TNF-α, IL-1β and IL-6), glial fibrillary acidic protein (GFAP), index of gliosis and neurodege…

0301 basic medicineMalemedicine.medical_specialtyInflammationmedicine.disease_causeDiet High-FatSettore BIO/09 - FisiologiaNeuroprotectionlcsh:RC321-57103 medical and health sciences0302 clinical medicineNeuroinflammationInternal medicinemedicineGlucagon-Like Peptide 2AnimalsObesityNeurodegenerationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroinflammationTUNEL assayGlial fibrillary acidic proteinbiologyChemistryNeurodegenerationdigestive oral and skin physiologyBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologyNeuroprotective AgentsNeurologyGliosisOxidative stressAstrocytesbiology.proteinGlucagon-Like Peptide-2 ReceptorOxidative streEncephalitismedicine.symptomInflammation MediatorsGLP-2030217 neurology & neurosurgeryOxidative stresshormones hormone substitutes and hormone antagonistsNeurobiology of disease
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Overactivation of the endocannabinoid system alters the antilipolytic action of insulin in mouse adipose tissue.

2017

Evidence has accumulated that obesity-related metabolic dysregulation is associated with overactivation of the endocannabinoid system (ECS), which involves cannabinoid receptor 1 (CB1R), in peripheral tissues, including adipose tissue (AT). The functional consequences of CB1R activation on AT metabolism remain unclear. Since excess fat mobilization is considered an important primary event contributing to the onset of insulin resistance, we combined in vivo and in vitro experiments to investigate whether activation of ECS could alter the lipolytic rate. For this purpose, the appearance of plasma glycerol was measured in wild-type and CB1R−/− mice after acute anandamide administration or inh…

0301 basic medicineMalemedicine.medical_specialtyPhysiologyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentAdipose tissue030209 endocrinology & metabolismBiologyFatty Acids NonesterifiedCANNABINOID RECEPTOR 103 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineInsulin resistanceDownregulation and upregulationReceptor Cannabinoid CB1Physiology (medical)Internal medicineinsulin resistancemedicineLipolysisAnimalsInsulinendocannabinoid systemInsulinHydrolysis[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismmedicine.diseaseEndocannabinoid systemUp-RegulationJZL195Mice Inbred C57BLcannabinoid receptor 1030104 developmental biologyEndocrinologychemistryAdipose TissuelipolysisJZL195Endocannabinoids
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Age-related regulation of bone formation by the sympathetic cannabinoid CB1 receptor.

2017

The endocannabinoid (eCB) system, including its receptors, ligands, and their metabolizing enzymes, plays an important role in bone physiology. Skeletal cannabinoid type 1 (CB1) receptor signaling transmits retrograde signals that restrain norepinephrine (NE) release, thus transiently stimulating bone formation following an acute challenge, suggesting a feedback circuit between sympathetic nerve terminals and osteoblasts. To assess the effect of chronic in vivo occurrence of this circuit, we characterized the skeletal phenotype of mice with a conditional deletion of the CB1 receptor in adrenergic/noradrenergic cells, including sympathetic nerves. Whereas the deletion of the CB1 receptor did…

0301 basic medicineMalemedicine.medical_specialtySympathetic nervous systemAgingHistologyCannabinoid receptorSympathetic Nervous SystemPhysiologyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentDopamine beta-HydroxylaseBone resorptionBone remodeling03 medical and health sciencesNorepinephrineNorepinephrineReceptor Cannabinoid CB1OsteogenesisInternal medicinemedicineAnimalsNeuropeptide YBone ResorptionReceptorMice KnockoutChemistryEndocannabinoid systemMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEndocrinologyCannabinoidReceptors Adrenergic beta-2Gene Deletionmedicine.drugEndocannabinoidsBone
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Sex hormones modulate pathogenic processes in experimental traumatic brain injury.

2018

Clinical and animal studies have revealed sex-specific differences in histopathological and neurological outcome after traumatic brain injury (TBI). The impact of perioperative administration of sex steroid inhibitors on TBI is still elusive. Here, we subjected male and female C57Bl/6N mice to the controlled cortical impact (CCI) model of TBI and applied pharmacological inhibitors of steroid hormone synthesis, that is, letrozole (LET, inhibiting estradiol synthesis by aromatase) and finasteride (FIN, inhibiting dihydrotestosterone synthesis by 5α-reductase), respectively, starting 72 h prior CCI, and continuing for a further 48 h after CCI. Initial gene expression analyses showed that andro…

0301 basic medicineMalemedicine.medical_specialtyanimal structuresmedicine.drug_classmedicine.medical_treatmentTropomyosin receptor kinase BTropomyosin receptor kinase ABiochemistryNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineInternal medicineBrain Injuries TraumaticmedicineAnimalsNerve Growth FactorsSex CharacteristicsbiologyEstradiolbusiness.industryEstrogen AntagonistsBrainDihydrotestosteroneAndrogennervous system diseasesMice Inbred C57BLSteroid hormoneDisease Models Animal030104 developmental biologyEndocrinologynervous systemSex steroidDihydrotestosteronebiology.proteinFemalebusiness030217 neurology & neurosurgeryNeurotrophinmedicine.drugJournal of neurochemistry
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Endothelial GLP-1 (Glucagon-Like Peptide 1) Receptor Mediates Cardiovascular Protection by Liraglutide In Mice With Experimental Arterial Hypertension

2019

Supplemental Digital Content is available in the text.

0301 basic medicineMalemedicine.medical_specialtyhypertensionBlotting WesternInflammationBlood Pressure030204 cardiovascular system & hematologyangiotensin IImedicine.disease_causeGlucagon-Like Peptide-1 Receptor1005403 medical and health sciencesMice0302 clinical medicine10030Internal medicinemedicineoxidative stressAnimalsHypoglycemic AgentsReceptor10111Cells CulturedMice KnockoutliraglutideLiraglutidebusiness.industryBasic SciencesType 2 Diabetes MellitusEndothelial CellsAtherosclerosisGlucagon-like peptide-1Angiotensin II3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology10040inflammationComputingMethodologies_DOCUMENTANDTEXTPROCESSINGRNAmedicine.symptomCardiology and Cardiovascular Medicinebusiness10024Oxidative stressmedicine.drug
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Decrease in αβ/γδ T-cell ratio is accompanied by a reduction in high-fat diet-induced weight gain, insulin resistance, and inflammation.

2018

The implication of αβ and γδ T cells in obesity-associated inflammation and insulin resistance (IR) remains uncertain. Mice lacking γδ T cells show either no difference or a decrease in high-fat diet (HFD)-induced IR, whereas partial depletion in γδ T cells does not protect from HFD-induced IR. αβ T-cell deficiency leads to a decrease in white adipose tissue (WAT) inflammation and IR without weight change, but partial depletion of these cells has not been studied. We previously described a mouse model overexpressing peroxisome proliferator-activated receptor β (PPAR-β) specifically in T cells [transgenic (Tg) T-PPAR-β] that exhibits a partial depletion in αβ T cells and no change in γδ T-ce…

0301 basic medicineMalemedicine.medical_specialtymedicine.medical_treatmentT cellReceptors Antigen T-Cell alpha-betaT-LymphocytesAdipose tissueInflammationWhite adipose tissueDiet High-FatWeight GainBiochemistry03 medical and health sciencesMice0302 clinical medicineImmune systemInsulin resistanceInternal medicineGlucose IntoleranceGeneticsmedicineAnimalsObesityMolecular BiologyInflammationChemistryInsulinWeight changeBody Weightfood and beveragesnutritional and metabolic diseasesReceptors Antigen T-Cell gamma-deltamedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologymedicine.anatomical_structurelipids (amino acids peptides and proteins)medicine.symptomInsulin Resistancehormones hormone substitutes and hormone antagonists030217 neurology & neurosurgeryBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Influence of endogenous glucagon-like peptide-2 on lipid disorders in mice fed a high-fat diet

2016

Aim: The purpose of the present study was to investigate the influence of endogenous glucagon-like peptide-2 (GLP-2) on lipid profile in mice fed a standard diet (STD) or a high-fat diet (HFD). Materials and methods: HFD- and age-matched STD mice were injected once a day with GLP-2 (3-33), a GLP-2 receptor (GLP-2R) antagonist, or vehicle for 4 weeks. Results: HFD mice displayed increased intrahepatic lipid concentration and hepatic steatosis and higher plasma concentrations of cholesterol, LDL, AST, and ALT than STD mice. No difference was observed in lipid fecal elimination. In STD mice, the chronic treatment with GLP-2 (3-33) did not affect any parameter, while in HFD mice, it enhanced pl…

0301 basic medicineMalemedicine.medical_specialtyobesityEndogenyBiologyDiet High-FatliverSettore BIO/09 - Fisiologia03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineInsulin resistanceEndocrinologyMetabolic DiseaseslipidInternal medicineinsulin resistancemedicineGlucagon-Like Peptide 2AnimalsReceptormedicine.diagnostic_testCholesterolSettore BIO/16 - Anatomia Umanadigestive oral and skin physiologyAntagonistGeneral Medicinemedicine.diseaseGlucagon-like peptide-2LipidsPeptide FragmentsMice Inbred C57BL030104 developmental biologyEndocrinologychemistrylipids (amino acids peptides and proteins)030211 gastroenterology & hepatologySteatosisLipid profileGLP-2hormones hormone substitutes and hormone antagonists
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Fate-Mapping of GM-CSF Expression Identifies a Discrete Subset of Inflammation-Driving T Helper Cells Regulated by Cytokines IL-23 and IL-1β.

2019

Summary Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pa…

0301 basic medicineMalemedicine.medical_treatmentImmunologyInterleukin-1betaInflammation610 Medicine & health10071 Functional Genomics Center ZurichBiology10263 Institute of Experimental Immunology03 medical and health sciencesInterferon-gammaMice0302 clinical medicineFate mappingImmunopathologymedicineInterleukin 23Immunology and AllergyAnimalsReceptorNeuroinflammationReceptors CXCR6InflammationMice KnockoutReceptors Interleukin-1 Type I2403 ImmunologyTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesReceptors InterleukinTh1 CellsPhenotype3. Good healthCell biology10040 Clinic for NeurologyMice Inbred C57BL030104 developmental biologyInfectious DiseasesCytokine030220 oncology & carcinogenesis2723 Immunology and AllergyInterleukin-23 Subunit p19570 Life sciences; biologyTh17 CellsFemalemedicine.symptomImmunity
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