Regulation of endothelial nitric oxide synthase: location, location, location

PW Shaul - Annual review of physiology, 2002 - annualreviews.org
PW Shaul
Annual review of physiology, 2002annualreviews.org
▪ Abstract Endothelial nitric oxide synthase (eNOS) is expressed in vascular endothelium,
airway epithelium, and certain other cell types where it generates the key signaling molecule
nitric oxide (NO). Diminished NO availability contributes to systemic and pulmonary
hypertension, atherosclerosis, and airway dysfunction. Complex mechanisms underly the
cell specificity of eNOS expression, and co-and post-translational processing leads to
trafficking of the enzyme to plasma membrane caveolae. Within caveolae, eNOS is the …
Abstract
Endothelial nitric oxide synthase (eNOS) is expressed in vascular endothelium, airway epithelium, and certain other cell types where it generates the key signaling molecule nitric oxide (NO). Diminished NO availability contributes to systemic and pulmonary hypertension, atherosclerosis, and airway dysfunction. Complex mechanisms underly the cell specificity of eNOS expression, and co- and post-translational processing leads to trafficking of the enzyme to plasma membrane caveolae. Within caveolae, eNOS is the downstream target member of a signaling complex in which it is functionally linked to both typical G protein-coupled receptors and less typical receptors such as estrogen receptor (ER) α and the high-density lipoprotein receptor SR-BI displaying novel actions. This compartmentalization facilitates dynamic protein-protein interactions and calcium- and phosphorylation-dependent signal transduction events that modify eNOS activity. Further understanding of these mechanisms will enable us to take preventive and therapeutic advantage of the powerful actions of NO in multiple cell types.
Annual Reviews