Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-3-6
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1340-3478
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
37-42
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Pitavastatin inhibits vascular smooth muscle cell proliferation by inactivating extracellular signal-regulated kinases 1/2.
pubmed:affiliation
Department of Endocrinology and Diabetes, Yokohama City University Medical Center, Yokohama, Japan. yamakat@urahp.yokohama-cu.ac.jp
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't