The inhibition of human mesangial cell proliferation by S-trans, trans-farnesylthiosalicylic acid

FTS (5-20 μmol/L) inhibits PDGF-induced but not serum-induced HMC proliferation. FTS (10-20 μmol/L) also promotes HMC apoptosis in the presence of PDGF but not serum. These effects appear to be mediated by inhibitory effects on Ras-dependent signaling that occur as a result of the dislodgment of Ras from its membrane-anchorage sites by FTS. The selectivity of FTS toward PDGF-driven HMC proliferation suggests that FTS may be a valuable therapeutic in mesangioproliferative renal disease.