Abstract：
AIMS:Insulin-like growth factor (IGF)-1 is a major mitogenic growth factor for mesangial cells (MCs). Statins slow the progression of chronic kidney disease by affecting inflammatory cell signaling pathways, in addition to improving lipid profile, however, no studies have investigated the effects of fluvastatin on mitogen-activated protein (MAP) kinase activity or MC proliferation in kidney cells. We investigated the effects of fluvastatin on IGF-1-induced activation of intracellular signal pathways and MC proliferation, and examined the inhibitory mechanisms of fluvastatin. MAIN METHODS:Western blotting and cell proliferation assay were used. KEY FINDINGS:IGF-1 induced phosphorylation of extracellular-related kinase (ERK)1/2, MAP or ERK kinase (MEK)1/2, and Akt, expression of cyclin D1, and MC proliferation in cultured human MCs. Fluvastatin or PD98059, an MEK1 inhibitor, completely abolished IGF-1-induced MEK1/2 and ERK1/2 phosphorylation and MC proliferation, whereas inhibition of Akt had no effect on MC proliferation. Mevalonic acid prevented fluvastatin inhibition of IGF-1-induced MEK1/2 and ERK1/2 phosphorylation, cyclin D1 expression, and MC proliferation. SIGNIFICANCE:Fluvastatin inhibits IGF-1-induced activation of the MAP kinase pathway and MC proliferation by mevalonic acid depletion, and might have renoprotective effects by inhibiting IGF-1-mediated MC proliferation.
journal_name
Life Scijournal_title
Life sciencesauthors
Shibata T,Tamura M,Kabashima N,Serino R,Tokunaga M,Matsumoto M,Miyamoto T,Miyazaki M,Furuno Y,Takeuchi M,Abe H,Okazaki M,Otsuji Ydoi
10.1016/j.lfs.2009.02.022subject
Has Abstractpub_date
2009-05-22 00:00:00pages
725-31issue
21-22eissn
0024-3205issn
1879-0631pii
S0024-3205(09)00094-0journal_volume
84pub_type
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