Search results for "C57BL"

showing 10 items of 1292 documents

Short-Term Effects of Microglia-Specific Mitochondrial Dysfunction on Amyloidosis in Transgenic Models of Alzheimer's Disease.

2018

Reduction of mitochondrial activity is a subtle and early event in the pathogenesis of Alzheimer’s disease. Mitochondrial damage and consequentially enhanced production of reactive oxygen species is particularly occurring in the vicinity of amyloid plaques. Since all cells are affected by mitochondrial damage, analyses of cell type-specific effects are challenging. To study the impact of mitochondrial alterations on microglial activity in a homogeneous genetic background, we generated bone marrow chimeras of irradiated 46-days-old APP-transgenic mice. For reconstitution, bone marrow from CX3CR1-eGFP mice with mitochondria of either non-obese diabetic or C57BL/6J animals was utilized. Succes…

0301 basic medicineMalePathologymedicine.medical_specialtyMitochondrial DiseasesAmyloidCellGreen Fluorescent ProteinsCX3C Chemokine Receptor 1Mice TransgenicPlaque AmyloidBiologyMitochondrionPathogenesis03 medical and health sciencesAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseMice Inbred NODCX3CR1medicinePresenilin-1AnimalsHumansMicrogliaGeneral NeuroscienceAmyloidosisCalcium-Binding ProteinsMicrofilament ProteinsGeneral MedicineAmyloidosismedicine.diseaseMitochondriaMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureFemaleBone marrowMicrogliaGeriatrics and Gerontology030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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CAMKIIγ suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis

2017

Atherosclerosis is the underlying etiology of cardiovascular disease, the leading cause of death worldwide. Atherosclerosis is a heterogeneous disease in which only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death. A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates these acute events. Here, we show that Ca2+/calmodulin-dependent protein kinase gamma (CaMKII gamma) in macrophages plays a major role in the development of necrotic, thin-capped plaques. Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation of CaMKII. We…

0301 basic medicineMalePathologymedicine.medical_specialtyPhagocytosisGene ExpressionInflammationApoptosisMice TransgenicBiologyPHAGOCYTOSISLIPID MEDIATORS03 medical and health sciencesNecrosisENDOPLASMIC-RETICULUM STRESSINFLAMMATIONCa2+/calmodulin-dependent protein kinaseC/EBP HOMOLOGOUS PROTEINmedicineMacrophageAnimalsHumansKINASE-IILiver X receptorEfferocytosisCells CulturedLiver X ReceptorsAPOE-DEFICIENT MICEc-Mer Tyrosine KinaseATF6MacrophagesAPOPTOTIC CELL ACCUMULATIONGeneral MedicineMERTKAtherosclerosisPlaque AtheroscleroticActivating Transcription Factor 6Enzyme ActivationMice Inbred C57BL030104 developmental biologyRESOLUTIONmedicine.symptomCalcium-Calmodulin-Dependent Protein Kinase Type 2LIVER-X-RECEPTORResearch ArticleSignal TransductionJournal of Clinical Investigation
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Oligodendrocytes Provide Antioxidant Defense Function for Neurons by Secreting Ferritin Heavy Chain.

2020

An evolutionarily conserved function of glia is to provide metabolic and structural support for neurons. To identify molecules generated by glia and with vital functions for neurons, we used Drosophila melanogaster as a screening tool, and subsequently translated the findings to mice. We found that a cargo receptor operating in the secretory pathway of glia was essential to maintain axonal integrity by regulating iron buffering. Ferritin heavy chain was identified as the critical secretory cargo, required for the protection against iron-mediated ferroptotic axonal damage. In mice, ferritin heavy chain is highly expressed by oligodendrocytes and secreted by employing an unconventional secret…

0301 basic medicineMalePhysiologyAntioxidantsArticlemetabolism [Oligodendroglia]03 medical and health sciencesMyelinMice0302 clinical medicineddc:570medicineAnimalsSecretionReceptorCytotoxicityMolecular BiologySecretory pathwayNeuronsbiologyChemistrymetabolism [Apoferritins]Cell Biologybiology.organism_classificationCell biologyFerritinMice Inbred C57BLOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemmetabolism [Neurons]Apoferritinsbiology.proteinmetabolism [Antioxidants]Drosophila melanogaster030217 neurology & neurosurgeryFunction (biology)Cell metabolism
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Circadian and Dopaminergic Regulation of Fatty Acid Oxidation Pathway Genes in Retina and Photoreceptor Cells.

2016

The energy metabolism of the retina might comply with daily changes in energy demand and is impaired in diabetic retinopathy-one of the most common causes of blindness in Europe and the USA. The aim of this study was to investigate putative adaptation of energy metabolism in healthy and diabetic retina. Hence expression analysis of metabolic pathway genes was performed using quantitative polymerase chain reaction, semi-quantitative western blot and immunohistochemistry. Transcriptional profiling of key enzymes of energy metabolism identified transcripts of mitochondrial fatty acid β-oxidation enzymes, i.e. carnitine palmitoyltransferase-1α (Cpt-1α) and medium chain acyl-CoA dehydrogenase (A…

0301 basic medicineMalePhysiologyDopamineMice ObeseGene Expressionlcsh:MedicineBiochemistryAcyl-CoA DehydrogenaseMice0302 clinical medicineCatecholaminesEndocrinologyMedicine and Health SciencesAminesEnzyme Chemistrylcsh:ScienceBeta oxidationMice KnockoutMice Inbred C3HMultidisciplinaryOrganic CompoundsDopaminergicFatty AcidsNeurochemistryDiabetic retinopathyNeurotransmittersCircadian RhythmChemistryCircadian Oscillatorsmedicine.anatomical_structurePhysical SciencesFemaleAnatomyOxidation-Reductionmedicine.drugResearch Articlemedicine.medical_specialtyBiogenic AminesEndocrine DisordersOcular AnatomyBiologyRetinaEnzyme Regulation03 medical and health sciencesOcular SystemInternal medicinemedicineGeneticsDiabetes MellitusAnimalsPhotoreceptor CellsGene RegulationCircadian rhythmCarnitineACADMRetinaDiabetic RetinopathyCarnitine O-PalmitoyltransferaseReceptor Melatonin MT1Receptors Dopamine D4Organic Chemistrylcsh:RChemical CompoundsBiology and Life Sciencesmedicine.diseaseHormonesMice Inbred C57BLMetabolic pathwayDisease Models Animal030104 developmental biologyEndocrinologyMetabolismMicroscopy FluorescenceMetabolic DisordersEnzymologylcsh:Qsense organsEnergy MetabolismPhysiological ProcessesChronobiology030217 neurology & neurosurgeryNeurosciencePLoS ONE
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The pituitary gland prevents shock-associated death by controlling multiple inflammatory mediators

2018

Abstract Bacterial infections cause a major burden of disease worldwide. Sepsis and septic shock are life-threatening complications of infections. The hypothalamic-pituitary-adrenal (HPA) axis initiates the release of endogenous glucocorticoids that modulate the host stress response and acute inflammation during septic shock. It is an ongoing controversial debate, if therapeutic manipulations of the HPA axis could benefit the clinical situation in the context of shock. Here, we have studied Long Evans rats with hypophysectomy followed by endotoxic shock. The shock-associated lethality was substantially higher in hypophysectomized rats as compared to control mice after cranial sham surgery (…

0301 basic medicineMalePituitary glandmedicine.medical_specialtyLipopolysaccharidemedicine.medical_treatmentBiophysicsInflammationBiochemistryArticleSepsis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinemedicineAnimalsRats Long-EvansMolecular BiologyInflammationSeptic shockbusiness.industryCell Biologymedicine.diseaseShock SepticMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEndocrinologyCytokinechemistry030220 oncology & carcinogenesisShock (circulatory)Pituitary GlandCytokinesTumor necrosis factor alphamedicine.symptomInflammation Mediatorsbusiness
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NKCC1-Mediated GABAergic Signaling Promotes Postnatal Cell Death in Neocortical Cajal-Retzius Cells.

2016

During early development, a substantial proportion of central neurons undergoes programmed cell death. This activity-dependent process is essential for the proper structural and functional development of the brain. To uncover cell type-specific differences in the regulation of neuronal survival versus apoptosis, we studied activity-regulated cell death in Cajal-Retzius neurons (CRNs) and the overall neuronal population in the developing mouse cerebral cortex. CRNs in the upper neocortical layer represent an early-born neuronal population, which is important for cortical development and largely disappears by apoptosis during neonatal stages. In contrast to the overall neuronal population, ac…

0301 basic medicineMaleProgrammed cell deathCognitive NeuroscienceApoptosisNeocortexReceptors Cell SurfaceBiologygamma-Aminobutyric acid03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicinemedicineAnimalsLectins C-TypeGABAergic NeuronsCells Culturedgamma-Aminobutyric AcidMice KnockoutNeocortexGABAA receptorDepolarizationInterstitial Cells of CajalReceptors GABA-AMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurenervous systemAnimals NewbornCerebral cortexApoptosisFemaleSignal transductionNeuroscience030217 neurology & neurosurgerymedicine.drugSignal TransductionCerebral cortex (New York, N.Y. : 1991)
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Androgen-inducible gene 1 increases the ER Ca(2+) content and cell death susceptibility against oxidative stress.

2016

Androgen-induced gene 1 (AIG1) is a transmembrane protein implicated with survival (its expression level was shown to correlate with the survival of patients suffering from hepatocellular carcinoma) and Ca(2+) signaling (over-expression of AIG1 increased transcription mediated by the Ca(2+)-dependent nuclear factor of activated T cells). We aimed to shed light on this less-studied protein and investigated its tissue expression, genomic organization, intracellular localization and membrane topology as well as its effects on cell death susceptibility and the Ca(2+) content of the endoplasmic reticulum. Immunoblotting of mouse tissues demonstrated highest expression of AIG1 in the liver, lung …

0301 basic medicineMaleProgrammed cell deathGene ExpressionBiologyEndoplasmic Reticulum03 medical and health sciencesMiceProtein DomainsGene expressionGeneticsAnimalsSex CharacteristicsCell DeathEndoplasmic reticulumMembrane ProteinsGeneral MedicineEmbryo MammalianMolecular biologyTransmembrane proteinCell biologyMice Inbred C57BLTransmembrane domainCytosolAlternative SplicingOxidative Stress030104 developmental biologyMembrane proteinOrgan SpecificityMembrane topologyCalciumFemaleGene
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Proteomic Analysis of Brain Region and Sex-Specific Synaptic Protein Expression in the Adult Mouse Brain

2020

Genetic disruption of synaptic proteins results in a whole variety of human neuropsychiatric disorders including intellectual disability, schizophrenia or autism spectrum disorder (ASD). In a wide range of these so-called synaptopathies a sex bias in prevalence and clinical course has been reported. Using an unbiased proteomic approach, we analyzed the proteome at the interaction site of the pre- and postsynaptic compartment, in the prefrontal cortex, hippocampus, striatum and cerebellum of male and female adult C57BL/6J mice. We were able to reveal a specific repertoire of synaptic proteins in different brain areas as it has been implied before. Additionally, we found a region-specific set…

0301 basic medicineMaleProteomicsCerebellumAgingcerebellumProteomehippocampusstriatumHippocampusNerve Tissue ProteinsBiologyArticleSynapse03 medical and health sciences0302 clinical medicinePostsynaptic potentialsynapsemedicinesexAnimalsPrefrontal cortexlcsh:QH301-705.5prefrontal cortexSex CharacteristicsBrainGeneral Medicinemedicine.diseaseMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Ontologylcsh:Biology (General)Autism spectrum disorderSchizophreniaProteomeSynapsesmass spectrometry-based proteomicsautism spectrum disorder (ASD)DDX3XFemaleNeuroscienceSET030217 neurology & neurosurgerySET ; cerebellum ; DDX3X ; striatum ; autism spectrum disorder (ASD) ; hippocampus ; synapse ; sex ; prefrontal cortexCells
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Functional role of endothelial CXCL16/CXCR6-platelet-leucocyte axis in angiotensin II-associated metabolic disorders.

2018

Aims Angiotensin-II (Ang-II) is the main effector peptide of the renin-angiotensin system (RAS) and promotes leucocyte adhesion to the stimulated endothelium. Because RAS activation and Ang-II signalling are implicated in metabolic syndrome (MS) and abdominal aortic aneurysm (AAA), we investigated the effect of Ang-II on CXCL16 arterial expression, the underlying mechanisms, and the functional role of the CXCL16/CXCR6 axis in these cardiometabolic disorders. Methods and results Results from in vitro chamber assays revealed that CXCL16 neutralization significantly inhibited mononuclear leucocyte adhesion to arterial but not to venous endothelial cells. Flow cytometry and immunofluorescence s…

0301 basic medicineMaleRHOAPhysiologyMice Knockout ApoE030204 cardiovascular system & hematology0302 clinical medicineLeukocytesReceptorCells CulturedMetabolic SyndromebiologyChemistryAngiotensin IIMiddle AgedAortic AneurysmVascular endothelial growth factor ALosartanmedicine.anatomical_structurecardiovascular systemFemaleCardiology and Cardiovascular Medicinemedicine.drugSignal TransductionAdultBlood Plateletsmedicine.medical_specialtyEndothelium03 medical and health sciencesPhysiology (medical)Internal medicinemedicineCell AdhesionAnimalsHumansPlatelet activationReceptors CXCR6Angiotensin II receptor type 1Endothelial CellsChemokine CXCL16Platelet ActivationAngiotensin IICoculture TechniquesMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyCase-Control Studiesbiology.proteinAngiotensin II Type 1 Receptor BlockersCardiovascular research
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Mast cells are associated with the onset and progression of celiac disease

2017

Background Celiac disease (CD) is an immune-mediated disorder characterized by an accumulation of immune cells in the duodenal mucosa as a consequence of both adaptive and innate immune responses to undigested gliadin peptides. Mast cells (MCs) are innate immune cells that are a major source of costimulatory signals and inflammatory mediators in the intestinal mucosa. Although MCs have previously been associated with CD, functional studies have never been performed. Objective We aimed at evaluating the role of MCs in the pathogenesis of CD. Methods Intestinal biopsy specimens of patients with CD were scored according to the Marsh classification and characterized for leukocyte infiltration a…

0301 basic medicineMaleSettore MED/09 - Medicina InternaImmunologygliadin immunologyFluorescent Antibody TechniqueBiologyCell DegranulationGliadinProinflammatory cytokinePathogenesis03 medical and health sciencesMice0302 clinical medicineImmune systemIntestinal mucosamedicineImmunology and AllergyAnimalsHumansCeliac diseaseMast CellsIntestinal Mucosap31-43 fragmentToll-like receptorInnate immune systemCeliac disease; gliadin immunology; mast cell; p31-43 fragment; mast cellFOXP3Mast cellImmunohistochemistryhumanitiesPeptide FragmentsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisImmunologyDisease ProgressionFemalemast cell
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