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Yamakawa, T. et al.

Yamakawa, Tanaka, Kamei, Kadonosono, Okuda,

Pitavastatin inhibits vascular smooth muscle cell proliferation by inactivating extracellular signal-regulated kinases 1/2.

We recently reported that lysophosphatidylcholine (lysoPC) acts on vascular smooth muscle cells ( VSMCs ) to produce a mitogenic response through the activation of extracellular signal-regulated kinases 1/2 (ERK1/2). In this study, we examined the role of HMG-CoA reductase inhibitors on lysoPC-induced VSMC proliferation. Pitavastatin, a new HMG-CoA reductase inhibitor, suppressed lysoPC-induced DNA synthesis in primary cultured rat VSMCs. Since lysoPC-induced ERK1/2 activation contributes to smooth muscle cell proliferation, we explored the effect of pitavastatin on ERK1/2 activation. Pitavastatin inhibited lysoPC-induced ERK1/2 phosphorylation and ERK1/2 activation. The other HMG-CoA reductase inhibitors, atrovastatin and fluvastatin, also inhibited lysoPC-induced ERK1/2 phosphorylation. Pitavastatin also inhibited lysoPC-induced c-fos mRNA expression. To gain insight into the mechanism of the inhibitory effect of pitavastatin on ERK1/2 activation by lysoPC, we examined the role of the mevalonate pathways. Mevalonate and farnesylpyrophosphate reduced the inhibition of ERK1/2 phosphorylation by pitavastatin. These studies demonstrate that pitavastatin may inhibit lysoPC-induced VSMC proliferation, at least in part, by inactivating ERK1/2, which is linked to mevalonate metabolism.[1]

References

Pitavastatin inhibits vascular smooth muscle cell proliferation by inactivating extracellular signal-regulated kinases 1/2. Yamakawa, T., Tanaka, S., Kamei, J., Kadonosono, K., Okuda, K. J. Atheroscler. Thromb. (2003) [Pubmed]

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