British Journal of Haematology · 2002 · 75 citations · 10 references
MedicineHematologyPhysiologyCellular MetabolismClinical BiochemistryHematology PhysiologyAnemiaHemoglobin PhysiologySickle Cell DiseaseCyclic Guanosine Monophosphate PathwayCyclic Guanosine Monophosphate SignalingHydroxyurea TherapyNitric OxideNitric Oxide BiologyNitric Oxide-mediated VasodilationProtein Kinase G SignalingSickle Cell Anemia
Recent studies suggest that nitric oxide (NO) may partly be responsible for the beneficial effect of hydroxyurea (HU) in sickle cell disease (SCD) patients. NO stimulates cyclic guanosine monophosphate (cGMP) production, which mediates vasodilatation. We investigated the association between NO, cGMP and fetal haemoglobin (HbF) levels after HU administration. Our data showed that chronic HU significantly increased NO, cGMP, and HbF levels in SCD. Recently it was shown that HbF production was stimulated by cGMP-dependent protein kinase. Our results suggest that NO stimulates cGMP production, which then activates a protein kinase and increases the production of HbF.
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Nitric oxide activates cyclooxygenase enzymes.
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