Uncoupling of endothelial nitric oxide synthase in cerebral vasculature of Tg2576 mice

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) (...

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Veröffentlicht in:Journal of neurochemistry 2015-09, Vol.134 (6), p.1129-1138
Hauptverfasser: Santhanam, Anantha Vijay R., d'Uscio, Livius V., He, Tongrong, Das, Pritam, Younkin, Steven G., Katusic, Zvonimir S.
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Sprache:eng
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Zusammenfassung: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 in cerebral vasculature of Tg2576 mice. In contrast, bioavailability of BH4 was significantly reduced (p 
ISSN:0022-3042
1471-4159
DOI:10.1111/jnc.13205