Hypoxia increases Hsp90 binding to eNOS via PI3K-Akt in porcine coronary artery endothelium
Hypoxia increases Hsp90 binding to eNOS via PI3K-Akt in porcine coronary artery endothelium
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DOI：
10.1038/labinvest.3700027
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发表时间：
2004-02-01
影响因子：
5
通讯作者：
Meyrick, B
中科院分区：
文献类型：
--
作者：
Chen, JX;Meyrick, B
本研究探讨了缺氧调节猪冠状动脉内皮细胞（PCAEC）磷酸化内皮型一氧化氮合酶（eNOS）活性和NO产生的分子机制。暴露于缺氧（pO（2）=10毫米汞柱）的时间长达3小时，导致eNOS蛋白表达的时间依赖性增加和早期（15分钟）和持续增加的eNOS磷酸化在Ser-1177。暴露于缺氧30分钟导致eNOS活性加倍（对照组=6.2 +/- 4.4 vs缺氧组=14.1 +/- 5.0 fmol cGMP/mug蛋白，P
This study examines the molecular mechanisms by which hypoxia regulates phosphorylated endothelial nitric oxide synthase (eNOS) activity and NO production in porcine coronary artery endothelial cells (PCAEC). Exposure to hypoxia (pO(2)=10 mmHg) for periods up to 3 h resulted in a time-dependent increase in eNOS protein expression and an early (15 min) and sustained increase in eNOS phosphorylation at Ser-1177. Exposure to hypoxia for 30 min led to a doubling in eNOS activity (control =6.2 +/- 4.4 vs hypoxia=14.1 +/- 5.0 fmol cGMP/mug protein, P