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In this study, we tested the hypothesis that reduced bioavailability of tetrahydrobiopterin (BH4) is a major mechanism responsible for pathogenesis of endothelial dysfunction in cerebral microvessels of transgenic mice expressing the Swedish double mutation of human amyloid precursor protein (APP) (Tg2576 mice). Endothelial nitric oxide synthase (eNOS) protein expression was significantly increased...
J. Neurochem. (2012) 122, 1211–1218.
AbstractIn this study, we used the GTP cyclohydrolase I‐deficient mice, i.e., hyperphenylalaninemic (hph‐1) mice, to test the hypothesis that the loss of tetrahydrobiopterin (BH4) in cerebral microvessels causes endothelial nitric oxide synthase (eNOS) uncoupling, resulting in increased superoxide anion production and inhibition of endothelial nitric oxide signaling...
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