The phosphorylation state of eNOS modulates vascular reactivity and outcome of cerebral ischemia in vivo

Authors

Dmitriy A. Atochin
Annie Wang
Victor W.T. Liu
Robin C. Looft-Wilson, William & MaryFollow

Document Type

Article

Department/Program

Kinesiology & Health Sciences

Journal Title

Journal of Clinical Investigation

Pub Date

7-2-2007

Publisher

American Society for Clinical Investigation

Volume

117

Issue

7

First Page

1961

Abstract

NO plays critical roles in vascular function. We show that modulation of the eNOS serine 1179 (S1179) phosphorylation site affects vascular reactivity and determines stroke size in vivo. Transgenic mice expressing only a phosphomimetic (S1179D) form of eNOS show greater vascular reactivity, develop less severe strokes, and have improved cerebral blood flow in a middle cerebral artery occlusion model than mice expressing an unphosphorylatable (S1179A) form. These results provide a molecular mechanism by which multiple diverse cardiovascular risks, such as diabetes and obesity, may be centrally integrated by eNOS phosphorylation in vivo to influence blood flow and cardiovascular disease. They also demonstrate the in vivo relevance of posttranslational modification of eNOS in vascular function.

Recommended Citation

Atochin, Dmitriy A.; Wang, Annie; Liu, Victor W.T.; and Looft-Wilson, Robin C., The phosphorylation state of eNOS modulates vascular reactivity and outcome of cerebral ischemia in vivo (2007). Journal of Clinical Investigation, 117(7), 1961-1967.
https://doi.org/10.1172/JCI29877

DOI

https://doi.org/10.1172/JCI29877