Hashiguchi Akihito, Yano Shigetoshi, Morioka Motohiro, Hamada Junichiro, Kochi Masato, Fukunaga Kohji
Department of Neurosurgery, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto City, Kumamoto, Japan.
Brain Res Mol Brain Res. 2005 Feb 18;133(2):317-9. doi: 10.1016/j.molbrainres.2004.10.042.
We investigated phosphorylation of endothelial nitric oxide synthase (eNOS) at two major sites, Ser1177 and Thr495, which has a critical role to control its activity, in the gerbil hippocampal microvasculature after transient forebrain ischemia. Ser1177 phosphorylation was unchanged by 24 h after reperfusion, despite post-ischemic up-regulation of eNOS protein. However, Thr495 phosphorylation significantly and persistently decreased by 48 h. We here defined the changes in eNOS phosphorylation in vivo following brain ischemia/reperfusion. (ischemia).
我们研究了短暂性前脑缺血后沙鼠海马微血管中内皮型一氧化氮合酶（eNOS）在两个主要位点Ser1177和Thr495的磷酸化情况，这两个位点对控制其活性起关键作用。尽管缺血后eNOS蛋白上调，但再灌注24小时后Ser1177磷酸化未发生变化。然而，Thr495磷酸化在48小时时显著且持续降低。我们在此明确了脑缺血/再灌注（缺血）后体内eNOS磷酸化的变化情况。
