TY - JOUR
T1 - Regulation of endothelial nitric oxide synthase
T2 - Location, location, location
AU - Shaul, Philip W.
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
KW - Caveolae
KW - Epithelium
KW - Estrogen
KW - High density lipoprotein
KW - Low density lipoprotein
UR - http://www.scopus.com/inward/record.url?scp=0036199988&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036199988&partnerID=8YFLogxK
U2 - 10.1146/annurev.physiol.64.081501.155952
DO - 10.1146/annurev.physiol.64.081501.155952
M3 - Review article
C2 - 11826287
AN - SCOPUS:0036199988
SN - 0066-4278
VL - 64
SP - 749
EP - 774
JO - Annual review of physiology
JF - Annual review of physiology
ER -