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Our study is designed to find what promotes the of adhesive lesions due to proliferation of epithelial proliferation of epithelial cells in Bowman’s capsule. cells of Bowman’s capsule, since FGF2 administration It has been reported recently that fibroblast growth caused an increase in PCNA-positive epithelial cells of factor 2 ( FGF2) has a proliferative eVect on cultured Bowman’s capsule and administration of the neutraglomerular epithelial cells [3]. Our study focused on lizing antibody inhibited the formation of adhesive the role of FGF2 in the formation of glomerular glomeruli. Furthermore, these findings indicate the adhesive lesions. Animal models with glomerular possibility that FGF2 will induce the podocyte injury. adhesive lesions were prepared by administering puromycin aminonucleoside (PAN ). In normal glomeruli, FGF2 staining was detected at the GBM and in the Why does FGF2 accelerate podocyte injury? mesangial areas. However, an increase of FGF2 staining in the cytoplasm of podocytes was observed in In contrast to mesangial cells and glomerular endothelial cells, podocytes have little proliferative capacity in PAN nephropathy. Furthermore, FGF2 and FGFR 1‐4 mRNAs were observed in both podocytes and vivo. The current consensus is that the mature podocyte is able to carry out limited DNA synthesis, but is epithelial cells of Bowman’s capsule. These findings suggest that FGF2 has an important role in the forma- unable to undergo cell division [5]. Our study attempted to compare PCNA-positive cells and bromotion of glomerular adhesive lesions. deoxyuridine (BrdU )-positive cells to ascertain the number of podocytes in PAN nephropathy. Also,

Cytokines and podocyte injury: the mechanism of fibroblast growth factor 2-induced podocyte injury