0000000000135549

AUTHOR

Irene Bosca

showing 2 related works from this author

Endothelial Nitric Oxide Synthase Regulates T Cell Receptor Signaling at the Immunological Synapse

2006

The role of nitric oxide (NO) in T cells remains controversial, and the origin and localization of endogenous NO and whether it regulates lymphocyte activation are unclear. We show here that, within minutes of binding to antigen, T cells produce NO via endothelial nitric oxide synthase (eNOS). This process required increased intracellular Ca2+ and phosphoinositide3-kinase activity. By using an eNOS-green fluorescent fusion protein and fluorescent probes to detect NO, we show that eNOS translocates with the Golgi apparatus to the immune synapse of T helper cells engaged with antigen-presenting cells (APC), where it was fully activated. Overexpression of eNOS prevented the central coalescence…

Interleukin 2CD3 ComplexNitric Oxide Synthase Type IIIT-LymphocytesImmunologyReceptors Antigen T-CellAntigen-Presenting CellsGolgi ApparatusBiologyLymphocyte ActivationNitric OxideNitric oxideImmunological synapseInterferon-gammaMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundAntigenmedicineAnimalsHumansImmunology and AllergyCytotoxic T cellAntigensMOLIMMUNOAntigen-presenting cellNitric Oxide Synthase Type IIIMice Mutant StrainsCell biologyInfectious DiseaseschemistryInterleukin-2CalciumSignal transductionSignal Transductionmedicine.drugImmunity
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Complex I dysfunction and tolerance to nitroglycerin: an approach based on mitochondrial-targeted antioxidants.

2006

Nitroglycerin (GTN) tolerance was induced in vivo (rats) and in vitro (rat and human vessels). Electrochemical detection revealed that the incubation dose of GTN (5×10 −6 mol/L) did not release NO or modify O 2 consumption when administered acutely. However, development of tolerance produced a decrease in both mitochondrial O 2 consumption and the K m for O 2 in animal and human vessels and endothelial cells in a noncompetitive action. GTN tolerance has been associated with impairment of GTN biotransformation through inhibition of aldehyde dehydrogenase (ALDH)-2, and with uncoupling of mitochondrial respiration. Feeding rats with mitochondrial-targeted antioxidants (mitoquinone [MQ]) and i…

MaleantioxidantAntioxidantPhysiologyUbiquinonemedicine.medical_treatmentMuscle RelaxationVasodilator AgentsAldehyde dehydrogenasePharmacologyMitochondrionmedicine.disease_causeAntioxidantsMuscle Smooth VascularRats Sprague-Dawleychemistry.chemical_compoundNitroglycerinDrug toleranceoxidative stressCyclic GMPchemistry.chemical_classificationbiologyAldehyde Dehydrogenase MitochondrialDrug ToleranceGlutathioneMitochondriamitochondriaBiochemistrycardiovascular systemCardiology and Cardiovascular Medicinecirculatory and respiratory physiologyMuscle ContractionendotheliumIn Vitro TechniquesMitochondrial ProteinsOrganophosphorus CompoundsOxygen ConsumptionRespirationmedicineAnimalsHumansReactive oxygen speciesElectron Transport Complex IDose-Response Relationship DrugEndothelial CellsGlutathioneAldehyde DehydrogenasenitroglycerinRatsOxidative Stresschemistrybiology.proteinReactive Oxygen SpeciesOxidative stressCirculation research
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