Supplementation of Nitric Oxide Attenuates AβPP and BACE1 Protein in Cerebral Microcirculation of eNOS-Deficient Mice

被引：36

作者：

Austin, Susan A.

d'Uscio, Livius V.

Katusic, Zvonimir S. ^{[1
,2
]}

机构：

[1] Mayo Clin, Dept Anesthesiol & Mol Pharmacol, Rochester, MN 55905 USA

[2] Mayo Clin, Dept Expt Therapeut, Rochester, MN 55905 USA

来源：

JOURNAL OF ALZHEIMERS DISEASE | 2013年 / 33卷 / 01期

基金：

美国国家卫生研究院;

关键词：

Alzheimer's disease; amyloid-beta; amyloid-beta protein precursor; endothelial nitric oxide synthase; nitric oxide; vascular endothelial cells; ALZHEIMERS-DISEASE; RISK; EXPRESSION; MECHANISM; SYNTHASE;

D O I：

10.3233/JAD-2012-121351

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Recently, we demonstrated in endothelial nitric oxide synthase deficient (eNOS(-/-)) mice that loss of endothelial NO led to increased protein levels of amyloid-beta protein precursor (A beta PP), beta-site A beta PP cleaving enzyme 1 (BACE1), and amyloid-beta (A beta) peptide. Therefore, our aim was to determine if NO supplementation in vivo would attenuate A beta PP and BACE1 protein levels. cGMP levels were significantly increased while A beta PP and BACE1 protein levels were statistically lower in cerebral microvessels from nitroglycerin-treated eNOS(-/-) mice as compared to vehicle-treated mice. Our findings support the concept that preservation of NO/cGMP signaling is an important modulator of expression and processing of A beta PP.

引用

页码：29 / 33

页数：5

共 14 条

[1]

Endothelial Nitric Oxide Modulates Expression and Processing of Amyloid Precursor Protein [J].