Figure 9.

Circulating FGF-2 precipitated the development of HIVAN in adult HIV-Tg₂₆ mice. WT and HIV-Tg₂₆ male adult mice without preexisting renal disease were infected with adenoviral viral vectors carrying a secreted form of human recombinant FGF-2 or the Lac-Z gene (n=5 per group) as described in Concise Methods. Renal sections were harvested 28 days after the adenoviral infection. (B and D) Both WT and HIV-Tg₂₆ mice infected with rAd-FGF-2 showed a significant recruitment of glomerular and tubular epithelial cells expressing proliferating cell nuclear antigen (PCNA), a marker of DNA synthesis, replication, and intrinsic repair activity when compared to mice (A and C) injected with rAd-LacZ vectors. (H) HIV-Tg₂₆ mice infected with rAd-FGF-2 showed a decreased number of WT-1⁺ cells compared with all other groups (E–G) (*P<0.01; ANOVA). (D and H) These changes were associated with the presence of FSGS lesions, tubular casts, and microcysts. The bar graphs show the immunohistochemistry staining scores corresponding to each group. Results are expressed as percent changes in PCNA or WT-1⁺ cells relative to the control group (WT mice infected with rAd-Lac-Z). Values significantly different from the corresponding control group are marked: *P<0.05; **P<0.01. Original magnification, ×200 in A–D; ×400 in E–H.