Search results for " Knockout"

showing 10 items of 764 documents

Regulation of Oxygen Distribution in Tissues by Endothelial Nitric Oxide

2009

Nitric oxide (NO) decreases cellular oxygen (O 2 ) consumption by competitively inhibiting cytochrome c oxidase. Here, we show that endogenously released endothelial NO, either basal or stimulated, can modulate O 2 consumption both throughout the thickness of conductance vessels and in the microcirculation. Furthermore, we have shown that such modulation regulates O 2 distribution to the surrounding tissues. We have demonstrated these effects by measuring O 2 consumption in blood vessels in a hypoxic chamber and O 2 distribution in the microcirculation using the fluorescent oxygen-probe Ru(phen) 3 2+ . Removal of NO by physical or pharmacological means, or in eNOS −/− mice, abolishes this …

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologychemistry.chemical_elementOxygen consumptionBiologyNitric OxideOxygenMicrocirculationNitric oxideElectron Transport Complex IVRats Sprague-DawleyMicechemistry.chemical_compoundOxygen Consumption:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]EnosInternal medicinemedicineAnimalsHumansCytochrome c oxidaseEndotheliumHypoxiaUNESCO::CIENCIAS MÉDICAS ::Medicina internaMice KnockoutNitric Oxide Synthase Type IIINitric oxide:CIENCIAS MÉDICAS [UNESCO]biology.organism_classificationRatsOxygenEndocrinologymedicine.anatomical_structurechemistryUNESCO::CIENCIAS MÉDICASCirculatory systemBiophysicsbiology.proteinNitric oxide ; Endothelium ; Oxygen consumptionEndothelium VascularCardiology and Cardiovascular MedicineSignal TransductionCirculation Research
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Chronic Therapy With Isosorbide-5-Mononitrate Causes Endothelial Dysfunction, Oxidative Stress and a Marked Increase in Vascular Endothelin-1 Express…

2011

Aims Isosorbide-5-mononitrate (ISMN) is one of the most frequently used compounds in the treatment of coronary artery disease predominantly in the USA. However, ISMN was reported to induce endothelial dysfunction, which was corrected by vitamin C pointing to a crucial role of reactive oxygen species (ROS) in causing this phenomenon. We sought to elucidate the mechanism how ISMN causes endothelial dysfunction and oxidative stress in vascular tissue. Methods and results Male Wistar rats ( n = 69 in total) were treated with ISMN (75 mg/kg/day) or placebo for 7 days. Endothelin (ET) expression was determined by immunohistochemistry in aortic sections. Isosorbide-5-mononitrate infusion caused si…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIIsosorbide DinitratePharmacologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesEnosInternal medicinePhysiology (medical)medicineAnimalsNitric Oxide DonorsEnzyme InhibitorsRats WistarEndothelial dysfunctionCyclic GMPAortaMice KnockoutNADPH oxidaseEndothelin-1biologybusiness.industryNADPH Oxidasesmedicine.diseasebiology.organism_classificationEndothelin 1BosentanRatsNitric oxide synthaseEndothelial stem cellOxidative StressNG-Nitroarginine Methyl EsterEndocrinologychemistryApocyninbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineEndothelin receptorbusinessOxidative stressSignal Transductionmedicine.drugFree Radical Biology and Medicine
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Modulation by NO of acetylcholine release in the ileum of wild-type and NOS gene knockout mice.

2002

Nitric oxide (NO) inhibits the release of acetylcholine and cholinergic contractions in the small intestine of several species, but no information is available about the mouse ileum. This study examines the effects of NO on the electrically evoked release of [3H]acetylcholine and smooth muscle contraction in myenteric plexus-longitudinal muscle preparations of wild-type mice and of neuronal NO synthase (nNOS) and endothelial NOS (eNOS) knockout mice. The NOS inhibitor N G-nitro-l-arginine (l-NNA) and the guanylyl cyclase inhibitor 1 H-[1,2,4]oxadiazolo[4,3-α]quinoxalin-1-one (ODQ) concentration dependently increased the evoked [3H]acetylcholine release and cholinergic contractions in prepa…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyNitric Oxide Synthase Type IIIleumNitric Oxide Synthase Type IBiologyIn Vitro TechniquesNitric OxideNitroarginineNitric oxidechemistry.chemical_compoundMiceIleumPhysiology (medical)Internal medicineQuinoxalinesmedicineAnimalsNitric Oxide DonorsEnzyme InhibitorsGene knockoutMice KnockoutOxadiazolesHepatologyPenicillamineGastroenterologyNitric Oxide Synthase Type IIISmall intestineAcetylcholineElectric StimulationNitric oxide synthaseEndocrinologymedicine.anatomical_structurechemistrybiology.proteinCholinergicNitric Oxide SynthaseGastrointestinal MotilityAcetylcholinemedicine.drugAmerican journal of physiology. Gastrointestinal and liver physiology
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Resveratrol Reverses Endothelial Nitric-Oxide Synthase Uncoupling in Apolipoprotein E Knockout Mice

2010

A crucial cause of the decreased bioactivity of nitric oxide (NO) in cardiovascular diseases is the uncoupling of the endothelial NO synthase (eNOS) caused by the oxidative stress-mediated deficiency of the NOS cofactor tetrahydrobiopterin (BH(4)). The reversal of eNOS uncoupling might represent a novel therapeutic approach. The treatment of apolipoprotein E knockout (ApoE-KO) mice with resveratrol resulted in the up-regulation of superoxide dismutase (SOD) isoforms (SOD1-SOD3), glutathione peroxidase 1 (GPx1), and catalase and the down-regulation of NADPH oxidases NOX2 and NOX4 in the hearts of ApoE-KO mice. This was associated with reductions in superoxide, 3-nitrotyrosine, and malondiald…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIISOD3SOD2ResveratrolAntioxidantsSuperoxide dismutaseMicechemistry.chemical_compoundApolipoproteins ESuperoxidesEnosMalondialdehydeInternal medicineStilbenesmedicineAnimalsGTP CyclohydrolaseMice KnockoutPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologyReverse Transcriptase Polymerase Chain ReactionSuperoxide DismutaseChemistrySuperoxideMyocardiumTetrahydrobiopterinbiology.organism_classificationBiopterinIsoenzymesOxidative StressEndocrinologyBiochemistryResveratrolbiology.proteinRNATyrosineMolecular Medicinemedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Oxytocin Regulates Neurosteroid Modulation of GABAAReceptors in Supraoptic Nucleus around Parturition

2003

In this study, we investigate how neurosteroid sensitivity of GABAAreceptors (GABAARs) is regulated. We examined this issue in neurons of the supraoptic nucleus (SON) of the rat and found that, during parturition, the GABAARs become insensitive to the neurosteroid allopregnanolone attributable to a shift in the balance between the activities of endogenous Ser/Thr phosphatase and PKC. In particular, a constitutive endogenous tone of oxytocin within the SON after parturition suppressed neurosteroid sensitivity of GABAARs via activation of PKC. Vice versa before parturition, during late pregnancy, application of exogenous oxytocin brings the GABAARs from a neurosteroid-sensitive mode toward a …

Malemedicine.medical_specialtyPatch-Clamp TechniquesNeuroactive steroidXenopusMice TransgenicPregnanoloneKidneyLigandsOxytocinTransfectionArticlegamma-Aminobutyric acidSupraoptic nucleusCell LineMicechemistry.chemical_compoundPregnancyInternal medicinemental disordersPhosphoprotein Phosphatasespolycyclic compoundsmedicineAnimalsHumansRats WistarProtein Kinase Cgamma-Aminobutyric AcidMice KnockoutPregnanoloneGABAA receptorGeneral NeuroscienceAllopregnanoloneKidney metabolismBridged Bicyclo Compounds HeterocyclicReceptors GABA-ARatsEndocrinologyAnimals Newbornnervous systemOxytocinchemistryOocytesFemaleSteroidsSupraoptic Nucleushormones hormone substitutes and hormone antagonistsmedicine.drugThe Journal of Neuroscience
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Differential cystine and dibasic amino acid handling after loss of function of the amino acid transporter b0,+ AT (Slc7a9) in mice

2013

Cystinuria is an autosomal recessive disease caused by mutations in SLC3A1 ( rBAT) and SLC7A9 ( b 0,+ AT). Gene targeting of the catalytic subunit ( Slc7a9) in mice leads to excessive excretion of cystine, lysine, arginine, and ornithine. Here, we studied this non-type I cystinuria mouse model using gene expression analysis, Western blotting, clearance, and brush-border membrane vesicle (BBMV) uptake experiments to further characterize the renal and intestinal consequences of losing Slc7a9 function. The electrogenic and BBMV flux studies in the intestine suggested that arginine and ornithine are transported via other routes apart from system b0,+. No remarkable gene expression changes were…

Malemedicine.medical_specialtyPeptide transporterArgininePhysiologyLysineCystineSLC7A9BiologyKidneyGFRMicechemistry.chemical_compoundInternal medicinemedicineAnimalsAmino acid transporterMice Knockoutchemistry.chemical_classificationKidneyCystinuriaAmino Acids DiaminoCystinuriaOrnithinemedicine.diseaseAmino acidMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureEndocrinologychemistryBiochemistryAmino Acid Transport Systems BasicCystineGlomerular Filtration Rate
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Paracrine Activation of Hepatic CB1 Receptors by Stellate Cell-Derived Endocannabinoids Mediates Alcoholic Fatty Liver

2008

SummaryAlcohol-induced fatty liver, a major cause of morbidity, has been attributed to enhanced hepatic lipogenesis and decreased fat clearance of unknown mechanism. Here we report that the steatosis induced in mice by a low-fat, liquid ethanol diet is attenuated by concurrent blockade of cannabinoid CB1 receptors. Global or hepatocyte-specific CB1 knockout mice are resistant to ethanol-induced steatosis and increases in lipogenic gene expression and have increased carnitine palmitoyltransferase 1 activity, which, unlike in controls, is not reduced by ethanol treatment. Ethanol feeding increases the hepatic expression of CB1 receptors and upregulates the endocannabinoid 2-arachidonoylglycer…

Malemedicine.medical_specialtyPhysiologyHUMDISEASEArachidonic AcidsGlyceridesMiceCarnitine palmitoyltransferase 1PiperidinesReceptor Cannabinoid CB1Internal medicineCannabinoid Receptor ModulatorsParacrine CommunicationmedicineAnimalsReceptorDiet Fat-RestrictedMolecular BiologyCells CulturedMice KnockoutCarnitine O-PalmitoyltransferaseEthanolChemistryLipogenesisFatty AcidsFatty liverCell Biologymedicine.diseaseEndocannabinoid systemCoculture TechniquesUp-RegulationMice Inbred C57BLDisease Models AnimalLipoprotein LipaseEndocrinologyLiverLipogenesisHepatocytesHepatic stellate cellPyrazoleslipids (amino acids peptides and proteins)Alcoholic fatty liverFatty Acid SynthasesRimonabantSteatosisSterol Regulatory Element Binding Protein 1Oxidation-ReductionEndocannabinoidsFatty Liver AlcoholicCell Metabolism
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Alterations in the Hippocampal Endocannabinoid System in Diet-Induced Obese Mice

2010

The endocannabinoid (eCB) system plays central roles in the regulation of food intake and energy expenditure. Its alteration in activity contributes to the development and maintenance of obesity. Stimulation of the cannabinoid receptor type 1 (CB1receptor) increases feeding, enhances reward aspects of eating, and promotes lipogenesis, whereas its blockade decreases appetite, sustains weight loss, increases insulin sensitivity, and alleviates dysregulation of lipid metabolism. The hypothesis has been put forward that the eCB system is overactive in obesity. Hippocampal circuits are not directly involved in the neuronal control of food intake and appetite, but they play important roles in hed…

Malemedicine.medical_specialtyPolyunsaturated Alkamidesmedicine.medical_treatmentmedia_common.quotation_subjectArachidonic AcidsBiologyHippocampusArticlegamma-Aminobutyric acidGlyceridesMice03 medical and health sciences0302 clinical medicineReceptor Cannabinoid CB1Internal medicineCannabinoid Receptor ModulatorsCannabinoid receptor type 1medicineAnimalsObesityReceptorgamma-Aminobutyric Acid030304 developmental biologymedia_commonMice KnockoutNeurons0303 health sciencesLong-Term Synaptic DepressionGeneral NeuroscienceAppetiteDietary FatsEndocannabinoid systemMice Inbred C57BLDisease Models AnimalLipoprotein LipaseEndocrinologynervous systemSynapsesSynaptic plasticitylipids (amino acids peptides and proteins)CannabinoidDiet-induced obese030217 neurology & neurosurgeryEndocannabinoidsmedicine.drugThe Journal of Neuroscience
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Adenosine A2A receptors in diffuse dermal fibrosis: pathogenic role in human dermal fibroblasts and in a murine model of scleroderma.

2006

Objective Adenosine regulates inflammation and tissue repair, and adenosine A2A receptors promote wound healing by stimulating collagen matrix production. We therefore examined whether adenosine A2A receptors contribute to the pathogenesis of dermal fibrosis. Methods Collagen production by primary human dermal fibroblasts was analyzed by real-time polymerase chain reaction, 14C-proline incorporation, and Sircol assay. Intracellular signaling for dermal collagen production was investigated using inhibitors of MEK-1 and by demonstration of ERK phosphorylation. In vivo effects were studied in a bleomycin-induced dermal fibrosis model using adenosine A2A receptor–deficient wild-type littermate …

Malemedicine.medical_specialtyReceptor Adenosine A2AImmunologyMAP Kinase Kinase 1Adenosine A2A receptorGene ExpressionBiologyMiceRheumatologyFibrosisInternal medicinemedicineImmunology and AllergyAnimalsHumansPharmacology (medical)RNA MessengerEnzyme InhibitorsReceptorCells CulturedMice Knockoutintegumentary systemTriazinesDermisPurinergic signallingFibroblastsTriazolesAdenosine A3 receptormedicine.diseaseAdenosineAdenosine receptorFibrosisMice Inbred C57BLDisease Models AnimalHydroxyprolineEndocrinologyScleroderma DiffuseCancer researchCollagenWound healingmedicine.drugArthritis and rheumatism
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Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: Implicatio…

2009

Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine acting on two distinct receptor subtypes, namely p55 and p75 receptors. TNF-alpha p55 and p75 receptor knockout mice were previously shown to display a decreased or enhanced susceptibility to seizures, respectively, suggesting intrinsic modifications in neuronal excitability. We investigated whether alterations in glutamate system function occur in these naive knockout mice with perturbed cytokine signaling that could explain their different propensity to develop seizures. Using Western blot analysis of hippocampal homogenates, we found that p55(-/-) mice have decreased levels of membrane GluR3 and NR1 glutamate receptor subuni…

Malemedicine.medical_specialtyReceptors Kainic acidMicrodialysisAction PotentialsGlutamic AcidKainate receptorAMPA receptorIn Vitro TechniquesBiologyHippocampusReceptors N-Methyl-D-Aspartateelectrophysiology microiontophoresisSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundGlutamatergicReceptors Kainic AcidSeizuresInternal medicinemedicineAnimalsReceptors Tumor Necrosis Factor Type IIReceptors AMPAMice KnockoutNeuronsInflammationTumor Necrosis Factor-alphaGeneral NeuroscienceGlutamate receptorProtein SubunitsEndocrinologymedicine.anatomical_structureReceptors Glutamatenervous systemchemistryReceptors Tumor Necrosis Factor Type IMetabotropic glutamate receptorAstrocytesCytokinesNMDA receptorNBQXDisease SusceptibilityAstrocyte
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