The phosphorylation state of eNOS modulates vascular reactivity and outcome of cerebral ischemia in vivo
Year: 2007
Type: article
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.
DOI: 10.1172/jci29877
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: NITRIC OXIDE SYNTHASE ISOFORMS IN ATHEROSCLEROSIS, G168696995, ATHEROSCLEROSIS AND CEREBRAL ISCHEMIA, INACTIVATION OF DELAYED RECTIFIER POTASSIUM CHANNELS, CO2 REMOVAL IN CLOSED LOOP VENTILATION SYSTEMS, Interdepartmental Stroke Program, Interdepartmental Stroke Program, eNOS phosphorylation in cerebrovascular function and stroke
OpenAlex ID: W2129753448