Abstract：
:Pitavastatin is a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor that is used for suppressing cholesterol biosynthesis. Previously, we have reported that pitavastatin induces the activation of endothelial nitric oxide synthase (eNOS) and increases nitric oxide (NO) production in vascular endothelial cells (EC). However, the mechanism of eNOS activation by pitavastatin remains unknown. Here, we examined the implications of pitavastatin-induced signaling in eNOS phosphorylation in EC. We found that treatment of EC with a low dose of pitavastatin induced eNOS phosphorylation at Ser-1177, activated Akt phosphorylation at Ser-473 in a time-and dose-dependent manner, and increased NO production. These processes were suppressed by the addition of either mevalonic acid (MEV) or geranylgeranyl pyrophosphate (GGPP). In addition, northern blot analysis revealed that pitavastatin did not increase eNOS mRNA expression level in EC. These results suggest that the activation of eNOS with a low dose of pitavastatin (0.1 microM) involves phosphoinositide 3-kinase and the Akt pathway and produces NO in EC, which is dependent on post-transcriptional regulation. This pathway is critical for cellular responses that contribute to EC function.
journal_name
Life Scijournal_title
Life sciencesauthors
Wang J,Tokoro T,Matsui K,Higa S,Kitajima Idoi
10.1016/j.lfs.2004.12.003subject
Has Abstractpub_date
2005-03-25 00:00:00pages
2257-68issue
19eissn
0024-3205issn
1879-0631pii
S0024-3205(05)00021-4journal_volume
76pub_type
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