Dephosphorylation of eNOS on Thr495 after transient forebrain ischemia in gerbil hippocampus

Akihito Hashiguchi; Shigetoshi Yano; Motohiro Morioka; Junichiro Hamada; Masato Kochi; Kohji Fukunaga

doi:10.1016/j.molbrainres.2004.10.042

Dephosphorylation of eNOS on Thr495 after transient forebrain ischemia in gerbil hippocampus

Akihito Hashiguchi, Shigetoshi Yano, Motohiro Morioka, Junichiro Hamada, Masato Kochi, Kohji Fukunaga

Research output: Contribution to journal › Article › peer-review

4 Citations (Scopus)

Abstract

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).

Original language	English
Pages (from-to)	317-319
Number of pages	3
Journal	Molecular Brain Research
Volume	133
Issue number	2
DOIs	https://doi.org/10.1016/j.molbrainres.2004.10.042
Publication status	Published - 2005 Feb 18
Externally published	Yes

Keywords

Cerebral ischemia
Nitric oxide
Phosphorylation
eNOS

ASJC Scopus subject areas

Molecular Biology
Cellular and Molecular Neuroscience

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10.1016/j.molbrainres.2004.10.042

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title = "Dephosphorylation of eNOS on Thr495 after transient forebrain ischemia in gerbil hippocampus",

abstract = "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).",

keywords = "Cerebral ischemia, Nitric oxide, Phosphorylation, eNOS",

author = "Akihito Hashiguchi and Shigetoshi Yano and Motohiro Morioka and Junichiro Hamada and Masato Kochi and Kohji Fukunaga",

note = "Funding Information: This study was supported in part by Grants-in Aid for Scientific Research from the ministry of Education, Science, Sports and Culture of Japan (S.Y., M.M., and K.F.).",

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doi = "10.1016/j.molbrainres.2004.10.042",

language = "English",

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journal = "Molecular Brain Research",

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T1 - Dephosphorylation of eNOS on Thr495 after transient forebrain ischemia in gerbil hippocampus

AU - Hashiguchi, Akihito

AU - Yano, Shigetoshi

AU - Morioka, Motohiro

AU - Hamada, Junichiro

AU - Kochi, Masato

AU - Fukunaga, Kohji

N1 - Funding Information: This study was supported in part by Grants-in Aid for Scientific Research from the ministry of Education, Science, Sports and Culture of Japan (S.Y., M.M., and K.F.).

PY - 2005/2/18

Y1 - 2005/2/18

N2 - 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).

AB - 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).

KW - Cerebral ischemia

KW - Nitric oxide

KW - Phosphorylation

KW - eNOS

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DO - 10.1016/j.molbrainres.2004.10.042

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JF - Molecular Brain Research

SN - 0006-8993

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Dephosphorylation of eNOS on Thr495 after transient forebrain ischemia in gerbil hippocampus

Abstract

Keywords

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