[Expression of FGF2, FGF receptor-1 and alpha-smooth muscle actin in experimental mesangial proliferative nephritis].

Mesangial cell (MC) proliferation is the principal cause of glomerulonephritis and glomerulosclerosis. Previous studies have demonstrated that various cytokines and growth factors are MC mitogens. In vitro, basic fibroblast growth factor (FGF2) stimulates MC proliferation. In the present study, two series of experiments were conducted using rats with anti-Thy 1.1 mesangial proliferative glomerulonephritis. The first series of experiments was designed to clarify the expression relationship between FGF2, FGF, receptor-1 (FGFR1) and alpha-smooth muscle actin (alpha-SMA). The second series examined the effect of intravenous administration of recombinant FGF2 in this model. The first series involving in situ hybridization with FGF2 and FGFR1 cRNA probes, showed that these mRNAs were expressed in the mesangial areas during the proliferative phase (days 4-7). Simultaneously, the alpha SMA scores of glomeruli also increased. In the second series, FGF2 was administered at 6, 12 and 24 hours (early group) and at 4, 5, and 6 days (late group) after disease induction. On day 7, there were more glomerular cells positive for proliferative cell nuclear antigen (PCNA) in the late group than in the control and early groups and the alpha-SMA scores of the glomeruli had increased in the late group. On day 14, the number of mesangial cells mainly increased in the late group. These findings suggest that FGF2 and FGFR1 showed significant correlation with the phenotypic changes of MC.