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Aldose reductase (AR), the first and the rate-limiting enzyme of the polyolpathway, has been implicated in platelet-derived growth factor (PDGF)-inducedproliferation of rat mesangial cells (MsCs). It is well known that AR plays animportant role in various chronic diabetic complications, for example, diabeticnephropathy. Moreover, our previous studies have demonstrated that an AR inhibitor(ARI) significantly reduced the proliferation of rat MsCs induced by PDGF, however,the mechanism remains unclear. The aim of the present study was to elucidate themolecular mechanisms through which AR regulates PDGF-induced rat MsC proliferation.It was demonstrated that PDGF-induced MsC proliferation was significantly inhibitedby pretreatment with ARI. Cell cycle analysis by flow cytometry revealed thatARI prevented the entry of cells from the G1 into the S phase. Furthermore, theeffect of the PI3K/Akt signaling pathway on the cell cycle was analyzed. The PI3K/Aktpathway was activated with PDGF treatment. However, ARI blocked Akt activationin response to PDGF. Moreover, PDGF increased the levels of p21Cip1 cyclin kinaseinhibitor protein in MsC, which was markedly inhibited by pretreatment with ARI.Conversely, PDGF significantly reduced the levels of the p27Kip1 cyclin kinaseinhibitor protein, which was also restored by pretreatment with ARI. In conclusion,AR is involved in PDGF-induced rat MsC proliferation, and may serve as a potentialtarget for the inhibition of MsC proliferation in several types of glomerulonephritis.

Aldose reductase regulates platelet-derived growth factor-induced proliferation through mediating cell cycle progression in rat mesangial cells