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. 2009 May 6;297(1):F85–F94. doi: 10.1152/ajprenal.90642.2008

Fig. 3.

Fig. 3.

Phosphatidylinositol 3-kinase (PI3K) mediates TGF-β1-stimulated MCP-1. A: a specific inhibitor of PI3K, LY294002 (25 μM), completely inhibited TGF-β-stimulated MCP-1 production by cultured podocytes (n = 3). The modest decrease in MCP-1 due to LY294002 alone was not significantly different from control. *P < 0.05 vs. control. †P < 0.05 vs. TGF-β. B: TGF-β1 treatment of podocytes activated the PI3K pathway, evident in the increased amount of phospho-Akt compared with the constant level of total Akt.