Tumor necrosis factor-[alpha ] inhibits insulin-induced increase in endothelial nitric oxide synthase and reduces insulin receptor content and phosphorylation in human aortic endothelial cells

Metabolism ◽  
2002 ◽  
Vol 51 (4) ◽  
pp. 487-491 ◽  
Author(s):  
Ahmad Aljada ◽  
Husam Ghanim ◽  
Ezzat Assian ◽  
Paresh Dandona
1997 ◽  
Vol 17 (10) ◽  
pp. 5719-5726 ◽  
Author(s):  
J Alonso ◽  
L Sánchez de Miguel ◽  
M Montón ◽  
S Casado ◽  
A López-Farré

Changes in endothelial nitric oxide synthase (eNOS) expression may be involved in the endothelium-dependent vasorelaxation dysfunction associated with several vascular diseases. In the present work, we demonstrate that eNOS mRNA contains a previously undescribed cis element in the 3' untranslated region (3' UTR). A U+C-rich segment in the 3' UTR is critical in complex formation with bovine aortic endothelial cell cytosolic proteins. Tumor necrosis factor alpha (TNF-alpha), which destabilizes eNOS mRNA, increased the binding activity of the cytosolic proteins in a time-dependent manner. These data suggest that endothelial cytosolic proteins bind to the 3' UTR of eNOS mRNA. These proteins may play a role in TNF-alpha-induced eNOS mRNA destabilization.


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