Dephosphorylation of eNOS on Thr495 after transient forebrain ischemia in gerbil hippocampus.
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).
Hashiguchi
Akihito
A
Department of Neurosurgery, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto City, Kumamoto, Japan. 000m9033@med.stud.kumamoto-u.ac.jp
Yano
Shigetoshi
S
Morioka
Motohiro
M
Hamada
Junichiro
J
Kochi
Masato
M
Fukunaga
Kohji
K
D000704:Analysis of Variance; D000818:Animals; D002452:Cell Count; D005849:Gerbillinae; D006624:Hippocampus / Q000378:metabolism*; D007150:Immunohistochemistry / Q000379:methods; D066298:In Vitro Techniques; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III; D010766:Phosphorylation; D015424:Reperfusion / Q000379:methods; D013912:Threonine / Q000378:metabolism*; D013997:Time Factors
D013912:Threonine; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III