Search results for " Knockout"

showing 10 items of 764 documents

Control of murine hair follicle regression (catagen) by TGF‐β1in vivo

2000

The regression phase of the hair cycle (catagen) is an apoptosis-driven process accompanied by terminal differentiation, proteolysis, and matrix remodeling. As an inhibitor of keratinocyte proliferation and inductor of keratinocyte apoptosis, transforming growth factor beta1 (TGF-beta1) has been proposed to play an important role in catagen regulation. This is suggested, for example, by maximal expression of TGF-beta1 and its receptors during late anagen and the onset of catagen of the hair cycle. We examined the potential involvement of TGF-beta1 in catagen control. We compared the first spontaneous entry of hair follicles into catagen between TGF-beta1 null mice and age-matched wild-type …

medicine.medical_specialtyApoptosisBiochemistryAndrologyMiceTransforming Growth Factor betaHair cycleInternal medicineIn Situ Nick-End LabelingGeneticsmedicineAnimalsHumansMolecular BiologyhirsutismMice KnockoutTUNEL assayintegumentary systembiologyChemistryTransforming growth factor betamedicine.diseaseHair follicleMice Inbred C57BLbody regionsmedicine.anatomical_structureEndocrinologybiology.proteinHuman hair growthKeratinocyteHair FollicleCell DivisionBiotechnologyTransforming growth factorThe FASEB Journal
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Dual specificity phosphatase 1 knockout mice show enhanced susceptibility to anaphylaxis but are sensitive to glucocorticoids.

2007

Dual specificity phosphatase DUSP1 (otherwise known as mitogen-activated phosphatase 1 or MKP-1) dephosphorylates MAPKs, particularly p38, and negatively regulates innate immunity. Recent studies have shown that the DUSP1 gene is transcriptionally up-regulated by glucocorticoids (GCs) and that the antiinflammatory action of GCs is impaired in DUSP1-/- mice. Here we show that GC-mediated dephosphorylation of ERK-1 and ERK-2 activated by IgE receptor cross-linking is unimpaired in bone marrow-derived mast cells (BMMCs) of DUSP1-/- mice. Dephosphorylation of phospho-p38 MAPK is impaired but only at early times of GC treatment. Proinflammatory cytokine and chemokine gene expression (CCL2, IL-6,…

medicine.medical_specialtyChemokinePhosphataseImmunoglobulin Ep38 Mitogen-Activated Protein KinasesProinflammatory cytokineDephosphorylationMiceEndocrinologyInternal medicineSepsisDual-specificity phosphatasemedicineAnimalsGenetic Predisposition to DiseaseMolecular BiologyAnaphylaxisGlucocorticoidsMice KnockoutMitogen-Activated Protein Kinase 1Mice Inbred C3HMitogen-Activated Protein Kinase 3biologyInterleukin-6Tumor Necrosis Factor-alphaDegranulationDual Specificity Phosphatase 1General MedicineMice Inbred C57BLEndocrinologyGene Expression RegulationMice Inbred DBAbiology.proteinCytokinesTumor necrosis factor alphaMolecular endocrinology (Baltimore, Md.)
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Role of the M3 Muscarinic Acetylcholine Receptor Subtype in Murine Ophthalmic Arteries After Endothelial Removal

2014

We tested the hypothesis that the M3 muscarinic acetylcholine receptor subtype mediates cholinergic responses in murine ophthalmic arteries after endothelial removal.Muscarinic receptor gene expression was determined in ophthalmic arteries with intact and with removed endothelium using real-time PCR. To examine the role of the M3 receptor in mediating vascular responses, ophthalmic arteries from M3 receptor-deficient mice (M3R(-/-)) and respective wild-type controls were studied in vitro. Functional studies were performed in nonpreconstricted arteries with either intact or removed endothelium using video microscopy.In endothelium-intact ophthalmic arteries, mRNA for all five muscarinic rece…

medicine.medical_specialtyEndotheliumReal-Time Polymerase Chain ReactionMiceOphthalmic ArteryRetinal DiseasesInternal medicineMuscarinic acetylcholine receptormedicineMuscarinic acetylcholine receptor M4AnimalsRNA MessengerMice KnockoutReceptor Muscarinic M3business.industryMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Muscarinic acetylcholine receptor M1ArticlesDisease Models AnimalEndocrinologymedicine.anatomical_structureGene Expression RegulationVasoconstrictioncardiovascular systemCholinergicEndothelium VascularbusinessAcetylcholinemedicine.drug
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Developmental and tumoral vascularization is regulated by G protein-coupled receptor kinase 2

2012

Tumor vessel dysfunction is a pivotal event in cancer progression. Using an in vivo neovascularization model, we identified G protein–coupled receptor kinase 2 (GRK2) as a key angiogenesis regulator. An impaired angiogenic response involving immature vessels was observed in mice hemizygous for Grk2 or in animals with endothelium-specific Grk2 silencing. ECs isolated from these animals displayed intrinsic alterations in migration, TGF-β signaling, and formation of tubular networks. Remarkably, an altered pattern of vessel growth and maturation was detected in postnatal retinas from endothelium-specific Grk2 knockout animals. Mouse embryos with systemic or endothelium-selective Grk2 ablation …

medicine.medical_specialtyG-Protein-Coupled Receptor Kinase 2Angiogenic SwitchAngiogenesisMedicinaActivin Receptors Type IIMelanoma ExperimentalReceptor Transforming Growth Factor-beta Type INeovascularization PhysiologicProtein Serine-Threonine KinasesBiologyMural cellGrk2Transforming Growth Factor beta1NeovascularizationMiceDownregulation and upregulationCell MovementPregnancyInternal medicinemedicineAnimalsHumansCell ProliferationHemizygoteMice KnockoutG protein-coupled receptor kinaseTumorNeovascularization PathologicEndothelial CellsRetinal VesselsG proteinGeneral MedicineCell biologyEndocrinologymedicine.anatomical_structurecardiovascular systemFemalePericyteSignal transductionmedicine.symptomActivin Receptors Type IReceptors Transforming Growth Factor betaSignal TransductionResearch Article
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Penicillin induced epileptiform activity and EEG spectrum analysis of BDNF heterozygous mice: an in vivo electrophysiological study.

2011

Brain-derived neurotrophic factor (BDNF) heterozygous mice (BDNF (+/-)) kindle slowly and have a higher seizure threshold. However, BDNF (+/-) mice exhibit reduced cortical inhibition and disrupted balance of excitation/inhibition synaptic transmission. We investigated penicillin-induced focal cortical epileptiform activity and electroencephalogram (EEG) spectral power of BDNF (+/-) mice, by using electrocorticogram (ECoG) recordings. BDNF (+/-) mice (n=10) and wild type littermates (n=9) were anesthetized with i.p. urethane (1.750g/kg). The recordings of ECoG were carried out by using a data acquisition system and 100IU penicillin was administered intracortically to induce epileptiform act…

medicine.medical_specialtyHeterozygoteMicroinjectionsMice TransgenicNeocortexPenicillinsElectroencephalographyNeurotransmissionMiceNeurotrophic factorsInternal medicinemedicineAnimalsCerebral CortexMice KnockoutEpilepsymedicine.diagnostic_testSeizure thresholdChemistryGeneral NeuroscienceBrain-Derived Neurotrophic FactorWild typeElectroencephalographyCortex (botany)Electrophysiological PhenomenaElectrophysiologyEndocrinologymedicine.anatomical_structurenervous systemCerebral cortexNeuroscienceBrain research bulletin
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Increased pain and neurogenic inflammation in mice deficient of neutral endopeptidase

2009

The complex regional pain syndrome (CRPS) is characterized by enhanced neurogenic inflammation, mediated by neuropeptides. Neutral endopeptidase (NEP) is a key enzyme in neuropeptide catabolism. We used NEP knock out (ko) mice to investigate whether NEP deficiency leads to increased pain behavior and signs of neurogenic inflammation after soft tissue trauma with and without nerve injury. After chronic constriction injury (CCI) of the right sciatic nerve, NEP ko mice were more sensitive to heat, to mechanical stimuli, and to cold than wild type mice. Tissue injury without nerve injury produced no differences between genotypes. After CCI, NEP ko mice showed increased hind paw edema but lower …

medicine.medical_specialtyHot TemperaturePainSubstance PEnzyme-Linked Immunosorbent AssayCalcitonin gene-related peptideSubstance PEndothelin 1lcsh:RC321-571chemistry.chemical_compoundMiceCGRP catabolismEdemaInternal medicinePhysical StimulationMedicineAnimalsEdemaMuscle SkeletalNeprilysinlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPain MeasurementSkinMice KnockoutNeurogenic inflammationEndothelin-1business.industryCCIfungiNerve injurymedicine.diseaseNeutral endopeptidaseEndothelin 1Sciatic NerveHindlimbCold TemperatureMice Inbred C57BLComplex regional pain syndromeEndocrinologyNeurologychemistryAnesthesiaNeprilysinmedicine.symptomNeurogenic InflammationbusinessSkin TemperaturePrimarily cold CRPSNeurobiology of Disease
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Impaired border zone formation and adverse remodeling after reperfused myocardial infarction in cannabinoid CB2 receptor deficient mice.

2014

Abstract Aims Reperfusion of myocardial infarction is associated with inflammatory reaction and subsequent myocardial remodeling with a rapid scar formation in mice. The cannabinoid receptor CB2 has been associated with cardioprotection and regulation of macrophage function. We investigated its role in remodeling of reperfused infarction. Main methods One hour LAD-occlusion was followed by reperfusion over 6 h and 1, 3 and 7 days in wild-type C57/BL6J (WT) and CB2 receptor-deficient (Cnr2 −/− ) mice (n = 8/group). Hearts were processed for functional, morphological and mRNA/protein analysis, and tissue concentration of endocannabinoids was determined using liquid chromatography-multiple rea…

medicine.medical_specialtyIschemiaMyocardial InfarctionInfarctionMyocardial Reperfusion InjuryGeneral Biochemistry Genetics and Molecular BiologyReceptor Cannabinoid CB2MiceInternal medicinemedicineCannabinoid receptor type 2AnimalsMyocytes CardiacMyocardial infarctionGeneral Pharmacology Toxicology and PharmaceuticsCardioprotectionInflammationMice KnockoutbiologyChemistryMyocardiumTenascin CHemodynamicsGranulation tissueGeneral Medicinemedicine.diseaseEndocannabinoid systemMice Inbred C57BLEndocrinologymedicine.anatomical_structureCardiologybiology.proteinGranulation TissueCytokinesLife sciences
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The CB1 cannabinoid receptor mediates excitotoxicity-induced neural progenitor proliferation and neurogenesis.

2007

Endocannabinoids are lipid signaling mediators that exert an important neuromodulatory role and confer neuroprotection in several types of brain injury. Excitotoxicity and stroke can induce neural progenitor (NP) proliferation and differentiation as an attempt of neuroregeneration after damage. Here we investigated the mechanism of hippocampal progenitor cell engagement upon excitotoxicity induced by kainic acid administration and the putative involvement of the CB1 cannabinoid receptor in this process. Adult NPs express kainate receptors that mediate proliferation and neurosphere generation in vitro via CB1 cannabinoid receptors. Similarly, in vivo studies showed that excitotoxicity-induce…

medicine.medical_specialtyKainic acidCannabinoid receptorNeurotoxinsExcitotoxicityKainate receptorBiologymedicine.disease_causeBiochemistryNeuroprotectionHippocampuschemistry.chemical_compoundMiceReceptor Cannabinoid CB1Epidermal growth factorInternal medicinemedicineAnimalsMolecular BiologyCell ProliferationMice KnockoutNeuronsKainic AcidStem CellsNeurogenesisCell BiologyEndocannabinoid systemCell biologyNerve RegenerationEndocrinologynervous systemchemistrylipids (amino acids peptides and proteins)Fibroblast Growth Factor 2The Journal of biological chemistry
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The deubiquitinating enzyme CYLD regulates the differentiation and maturation of thymic medullary epithelial cells.

2014

The cross talk between thymocytes and the thymic epithelium is critical for T-cell development and the establishment of central tolerance. Medullary thymic epithelial cells (mTECs) are located in the thymic medulla and mediate the elimination of self-reactive thymocytes, thereby preventing the onset of autoimmunity. Previous studies identified the deubiquitinating enzyme CYLD as a critical regulator of T-cell development by activating proximal T-cell receptor signaling during the transition of double-positive to single-positive thymocytes. Here we evaluated the impact of the naturally occurring short-splice variant of the cyld gene (sCYLD) on the development and maturation of mTECs. We foun…

medicine.medical_specialtyMedullary cavityImmunologyReceptors Antigen T-CellCell CountThymus GlandBiologyDeubiquitinating Enzyme CYLDImmunophenotypingMiceInternal medicinemedicineImmunology and AllergyAnimalsMice KnockoutThymocytesUbiquitinationCell DifferentiationEpithelial CellsCell BiologyCell biologyDeubiquitinating Enzyme CYLDCysteine EndopeptidasesEndocrinologyPhenotypeAntigens SurfaceMutationFemaleSignal TransductionImmunology and cell biology
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Stabilization of Perivascular Mast Cells by Endothelial CNP (C-Type Natriuretic Peptide)

2020

Objective: Activated perivascular mast cells (MCs) participate in different cardiovascular diseases. Many factors provoking MC degranulation have been described, while physiological counterregulators are barely known. Endothelial CNP (C-type natriuretic peptide) participates in the maintenance of vascular barrier integrity, but the target cells and mechanisms are unclear. Here, we studied whether MCs are regulated by CNP. Approach and Results: In cultured human and murine MCs, CNP activated its specific GC (guanylyl cyclase)-B receptor and cyclic GMP signaling. This enhanced cyclic GMP–dependent phosphorylation of the cytoskeleton-associated VASP (vasodilator-stimulated phosphoprotein) and…

medicine.medical_specialtyMice 129 StrainMedizinMyocardial Reperfusion InjuryCell DegranulationCell LineMicrocirculationCapillary PermeabilityCyclic gmpAdenosine TriphosphateInternal medicineParacrine CommunicationmedicineAnimalsMast CellsPhosphorylationCyclic GMPMice KnockoutChemistryMicrofilament ProteinsDegranulationEndothelial CellsNatriuretic Peptide C-TypeThrombosisPhosphoproteinsMice Inbred C57BLDisease Models AnimalEndocrinologyNeutrophil InfiltrationC-type natriuretic peptideCardiology and Cardiovascular MedicineCell Adhesion MoleculesReceptors Atrial Natriuretic FactorSignal TransductionGuanylate cyclase
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