Search results for "inbred c57bl"

showing 10 items of 1287 documents

Creating a conditional mutation of Wnt-1 by antisense transgenesis provides evidence that Wnt-1 is not essential for spermatogenesis.

1993

We have used mice transgenic for an antisense construct for Wnt-1 to study the role of this gene in post-meiotic sperm development. The human PGK-2 promoter provided levels of Wnt-1 antisense mRNA in testes in 5 transgenic lines greatly in excess of Wnt-1 mRNA concentrations, and Wnt-1 mRNA levels were greatly decreased in the lines, by 98% in three of them. There was a general correlation between copy number of the insert, levels of antisense RNA, and decreases in mRNA. There was little effect of the antisense transgene on fertility or testicular histology suggesting that normal levels of Wnt-1 transcript are not essential for spermatogenesis.

MaleTransgeneRecombinant Fusion ProteinsMolecular Sequence DataMice Inbred StrainsMice TransgenicWnt1 ProteinBiologyMiceProto-Oncogene ProteinsGene expressionTestisGeneticsAnimalsRNA AntisenseRNA MessengerPromoter Regions GeneticSpermatogenesisRegulation of gene expressionMice KnockoutMessenger RNABase SequenceWnt signaling pathwayRNACell BiologyZebrafish ProteinsMolecular biologyAntisense RNATransgenesisMice Inbred C57BLWnt ProteinsPhosphoglycerate KinaseFertilityGene Expression RegulationOrgan SpecificityDevelopmental BiologyDevelopmental genetics
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2-Methoxyestradiol confers neuroprotection and inhibits a maladaptive HIF-1α response after traumatic brain injury in mice

2014

HIF-1α is pivotal for cellular homeostasis in response to cerebral ischemia. Pharmacological inhibition of HIF-1α may reduce secondary brain damage by targeting post-translational mechanisms associated with its proteasomal degradation and nuclear translocation. This study examined the neuroprotective effects of 2-methoxyestradiol (2ME2), the involved HIF-1α-dependent response, and alternative splicing in exon 14 of HIF-1α (HIF-1α∆Ex14) after traumatic brain injury (TBI) in mice. Intraperitoneal 2ME2 administration 30 min after TBI caused a dose-dependent reduction in secondary brain damage after 24 h. 2ME2 was physiologically tolerated, showed no effects on immune cell brain migration, and …

MaleTraumatic brain injuryBlotting WesternIschemiaCellular homeostasisBrain damagePharmacologyBiologyBiochemistryNeuroprotectionBrain IschemiaMitochondrial ProteinsMiceCellular and Molecular Neurosciencechemistry.chemical_compoundPlasminogen Activator Inhibitor 1medicineAnimalsCell NucleusNeuronsEstradiolTumor Necrosis Factor-alphaAlternative splicingMembrane ProteinsExonsHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseImmunohistochemistryUp-RegulationMice Inbred C57BLAlternative SplicingProtein TransportNeuroprotective AgentsGene Expression RegulationchemistryBrain InjuriesPlasminogen activator inhibitor-1Tumor necrosis factor alphamedicine.symptomNeuroscienceInjections IntraperitonealSubcellular FractionsJournal of Neurochemistry
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The antioxidative, non-psychoactive tricyclic phenothiazine reduces brain damage after experimental traumatic brain injury in mice.

2014

Abstract Oxidative stress due to free radical formation is an important mechanism of secondary brain damage following traumatic brain injury (TBI). Phenothiazine has been found to be a strong antioxidant in eukaryotic cells in vitro and in invertebrates in vivo. The present study was designed to determine the neuroprotective potency of unsubstituted phenothiazine in a paradigm of acute brain injury. Thirty minutes after pneumatic, controlled cortical impact (CCI) injury, C57BI6 mice were randomly assigned to “low dose” (3 mg/kg, LD) or “high dose” (30 mg/kg, HD) s.c. phenothiazine or vehicle treatment. Brain lesion, neurofunctional impairment, body weight, and markers of cerebral inflammati…

MaleTraumatic brain injuryGene ExpressionInflammationCell CountBrain damagePharmacologymedicine.disease_causeNeuroprotectionAntioxidantsRandom AllocationIn vivoPhenothiazinesMedicineAnimalschemistry.chemical_classificationInflammationDose-Response Relationship Drugbusiness.industryGeneral NeuroscienceCalcium-Binding ProteinsMicrofilament ProteinsBrainmedicine.diseaseMice Inbred C57BLchemistryAnesthesiaBrain InjuriesTumor necrosis factor alphamedicine.symptombusinessNeurogliaOxidative stressTricyclicNeuroscience letters
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Glucocorticoid receptor knockdown decreases the antioxidant protection of B16 melanoma cells: an endocrine system-related mechanism that compromises …

2014

We previously reported an interorgan system in which stress-related hormones (corticosterone and noradrenaline), interleukin-6, and glutathione (GSH) coordinately regulate metastatic growth of highly aggressive B16-F10 melanoma cells. Corticosterone, at levels measured in tumor-bearing mice, also induces apoptotic cell death in metastatic cells with low GSH content. In the present study we explored the potential role of glucocorticoids in the regulation of metastatic cell death/survival during the early stages of organ invasion. Glucocorticoid receptor (GCR) knockdown decreased the expression and activity of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting step in GSH synthesis, in …

MaleTumor PhysiologyGlutathione reductaseCancer TreatmentMelanoma ExperimentalGene Expressionlcsh:MedicineBiochemistryAntioxidantsMetastasisAnalytical Chemistrychemistry.chemical_compoundOxidative DamageMiceGlucocorticoid receptorSpectrum Analysis TechniquesCell SignalingNeoplasmsMolecular Cell BiologyBasic Cancer ResearchMedicine and Health SciencesNeoplasm Metastasislcsh:Sciencechemistry.chemical_classificationMultidisciplinaryCell DeathGlutathione peroxidaseEndocrine TherapyFlow CytometryGlutathioneChemistrymedicine.anatomical_structureOncologyResearch DesignSpectrophotometryPhysical SciencesCytophotometryGlucocorticoidmedicine.drugResearch ArticleSignal Transductionmedicine.medical_specialtyEndotheliumClinical Research DesignCell SurvivalGlutamate-Cysteine LigaseDown-RegulationEndocrine SystemBiologyResearch and Analysis MethodsCell LineReceptors GlucocorticoidInternal medicineCell Line TumormedicineGeneticsAnimalsHumansAnimal Models of DiseaseOncogenic Signalinglcsh:RBiology and Life SciencesEndothelial CellsGlutathioneCell BiologyMice Inbred C57BLEndocrinologyHEK293 CellschemistryCell cultureCancer cellAnimal Studieslcsh:QEndothelium VascularCytometryPLoS ONE
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Modulation of Exposure to Static Magnetic Field Affects Targeted Therapy of Solid Tumors In Vivo

2018

Background Static magnetic fields (SMF) exhibit antitumoral activity and enhance the efficacy of chemotherapy by opening the tumor-blood barrier. This study aimed to analyze different SMF-exposure protocols on epidermal growth factor receptor (EGFR)-overexpressing tumors, as well as their combination with cetuximab. Materials and methods Experiments were performed in skinfold chamber preparations of C57Bl/6-and CD-1nu/nu mice bearing LLC-1 tumors. Animals were exposed to 587 mT magnetic field following different exposure protocols. A subgroup received additional cetuximab injections. Using in vivo-fluorescence microscopy and planimetry, tumor angiogenesis, growth and microcirculation were r…

MaleTumor angiogenesisCancer ResearchAngiogenesismedicine.medical_treatmentCetuximabMice Nude02 engineering and technology030218 nuclear medicine & medical imagingMicrocirculationTargeted therapyMice03 medical and health sciences0302 clinical medicineIn vivoNeoplasmsLeukocytesmedicineAnimalsEndotheliumEpidermal growth factor receptorCell ProliferationChemotherapyNeovascularization PathologicCetuximabbiologybusiness.industryMicrocirculationGeneral Medicine021001 nanoscience & nanotechnologyErbB ReceptorsMice Inbred C57BLMagnetic FieldsOncologyCancer researchbiology.protein0210 nano-technologybusinessmedicine.drugAnticancer Research
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Suppression of the JNK Pathway by Induction of a Metabolic Stress Response Prevents Vascular Injury and Dysfunction

2008

Background— Oxidative injury and dysfunction of the vascular endothelium are early and causal features of many vascular diseases. Single antioxidant strategies to prevent vascular injury have met with mixed results. Methods and Results— Here, we report that induction of a metabolic stress response with adenosine monophosphate kinase (AMPK) prevents oxidative endothelial cell injury. This response is characterized by stabilization of the mitochondrion and increased mitochondrial biogenesis, resulting in attenuation of oxidative c-Jun N-terminal kinase (JNK) activation. We report that peroxisome proliferator coactivator 1α is a key downstream target of AMPK that is both necessary and suffici…

MaleUmbilical Veinsmedicine.medical_specialtyEndotheliumMitochondrionmedicine.disease_causeArticleMiceInternal medicinePhysiology (medical)Chlorocebus aethiopsmedicineAnimalsHumansVascular DiseasesRNA Small InterferingEndothelial dysfunctionHeat-Shock ProteinsMembrane Potential MitochondrialCell Deathbusiness.industryAdenylate KinaseJNK Mitogen-Activated Protein KinasesEndothelial CellsAMPKHydrogen PeroxideRibonucleotidesAminoimidazole CarboxamideOxidantsmedicine.diseaseAdaptation PhysiologicalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAngiotensin IICell biologyMice Inbred C57BLEndothelial stem cellOxidative Stressmedicine.anatomical_structureEndocrinologyMitochondrial biogenesisMutagenesisCOS CellsbusinessCardiology and Cardiovascular MedicineOxidative stressTranscription FactorsCirculation
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Vitamin D Receptor Activation Reduces Angiotensin-II–Induced Dissecting Abdominal Aortic Aneurysm in Apolipoprotein E–Knockout Mice

2015

Objective— Abdominal aortic aneurysm (AAA) is a vascular disorder characterized by chronic inflammation of the aortic wall. Low concentrations of vitamin D 3 are associated with AAA development; however, the potential direct effect of vitamin D 3 on AAA remains unknown. This study evaluates the effect of oral treatment with the vitamin D 3 receptor (VDR) ligand, calcitriol, on dissecting AAA induced by angiotensin-II (Ang-II) infusion in apoE −/− mice. Approach and Results— Oral treatment with calcitriol reduced Ang-II–induced dissecting AAA formation in apoE −/− mice, which was unrelated to systolic blood pressure or plasma cholesterol concentrations. Immunohistochemistry and reverse-tran…

MaleVascular Endothelial Growth Factor A0301 basic medicineDissecting Abdominal Aortic Aneurysm030204 cardiovascular system & hematologyLigandsCalcitriol receptorchemistry.chemical_compound0302 clinical medicineAorta AbdominalCells CulturedMice KnockoutAngiotensin IIVascular endothelial growth factorChemotaxis LeukocyteVascular endothelial growth factor APhenotypeMatrix Metalloproteinase 9Vitamin D3 ReceptorMatrix Metalloproteinase 2RNA Interferencelipids (amino acids peptides and proteins)ChemokinesMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineSignal Transductionmedicine.drugmedicine.medical_specialtyCalcitriolBiologyTransfectionProinflammatory cytokine03 medical and health sciencesApolipoproteins ECalcitriolInternal medicineHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansGenetic Predisposition to DiseaseRetinoid X Receptor alphaMacrophagesAngiotensin IIMice Inbred C57BLAortic DissectionDisease Models Animal030104 developmental biologyEndocrinologychemistryReceptors CalcitriolAortic Aneurysm AbdominalArteriosclerosis, Thrombosis, and Vascular Biology
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Engineered microenvironments for synergistic VEGF - Integrin signalling during vascularization

2017

We have engineered polymer-based microenvironments that promote vasculogenesis both in vitro and in vivo through synergistic integrin-growth factor receptor signalling. Poly(ethyl acrylate) (PEA) triggers spontaneous organization of fibronectin (FN) into nanonetworks which provide availability of critical binding domains. Importantly, the growth factor binding (FNIII12-14) and integrin binding (FNIII9-10) regions are simultaneously available on FN fibrils assembled on PEA. This material platform promotes synergistic integrin/VEGF signalling which is highly effective for vascularization events in vitro with low concentrations of VEGF. VEGF specifically binds to FN fibrils on PEA compared to …

MaleVascular Endothelial Growth Factor AIntegrinsBiophysicsNeovascularization PhysiologicBioengineeringpoly(ethyl acrylate)ArticleBiomaterialsHuman Umbilical Vein Endothelial CellsImage Processing Computer-AssistedAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesFibronectinTissue EngineeringPhospholipase C gammaProtein assemblyVascularizationVEGFFibronectinsMice Inbred C57BLCellular MicroenvironmentMechanics of MaterialsFocal Adhesion Protein-Tyrosine KinasesFISICA APLICADAMutationCeramics and CompositesINGENIERIA ELECTRICAGrowth factorsProtein BindingSignal Transduction
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Angiogenesis in Wounds Treated by Microdeformational Wound Therapy.

2011

BACKGROUND:: Mechanical forces play an important role in tissue neovascularization and are a constituent part of modern wound therapies. The mechanisms by which vacuum assisted closure (VAC) modulates wound angiogenesis are still largely unknown. OBJECTIVE:: To investigate how VAC treatment affects wound hypoxia and related profiles of angiogenic factors as well as to identify the anatomical characteristics of the resultant, newly formed vessels. METHODS:: Wound neovascularization was evaluated by morphometric analysis of CD31-stained wound cross-sections as well as by corrosion casting analysis. Wound hypoxia and mRNA expression of HIF-1α and associated angiogenic factors were evaluated by…

MaleVascular Endothelial Growth Factor APathologymedicine.medical_specialtyWound therapyAngiogenesismedicine.medical_treatmentNeovascularization PhysiologicOcclusive DressingsArticleNeovascularizationMiceNegative-pressure wound therapymedicineAnimalsSkinWound Healingintegumentary systemReverse Transcriptase Polymerase Chain Reactionbusiness.industryGranulation tissueBiomechanical PhenomenaMice Inbred C57BLOxygenPlatelet Endothelial Cell Adhesion Molecule-1Occlusive dressingVascular endothelial growth factor Amedicine.anatomical_structureMicrovesselsGranulation TissueCancer researchSurgerymedicine.symptombusinessWound healingNegative-Pressure Wound Therapy
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Quantitation of Microcomputed Tomography-Imaged Ocular Microvasculature

2010

To quantitatively assess microvascular dimensions in the eyes of neonatal wild-type and VEGF(120)-tg mice, using a novel combination of techniques which permit three-dimensional (3D) image reconstruction.A novel combination of techniques was developed for the accurate 3D imaging of the microvasculature and demonstrated on the hyaloid vasculature of the neonatal mouse eye. Vascular corrosion casting is used to create a stable replica of the vascular network and X-ray microcomputed tomography (muCT) to obtain the 3D images. In-house computer-aided image analysis techniques were then used to perform a quantitative morphological analysis of the images.With the use of these methods, differences …

MaleVascular Endothelial Growth Factor APathologymedicine.medical_specialtyX-ray microtomographyPhysiologyVEGF receptorsGene ExpressionMice TransgenicIterative reconstructionCorrosion CastingEyeMiceImaging Three-DimensionalPhysiology (medical)medicineAnimalsProtein IsoformsMolecular Biologybiologybusiness.industryMicrocirculationMicro computed tomographyX-Ray MicrotomographyMicrocomputed tomographyCapillariesMice Inbred C57BLPhenotypeAnimals NewbornMicroscopy Electron Scanningbiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessBiomedical engineeringMicrocirculation
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