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. 2009 Mar;20(3):554–566. doi: 10.1681/ASN.2008040445

Figure 5.

Figure 5.

PI3K is required for PKC-β1 activation and downstream signaling. MCs were treated with the PI3K inhibitors wortmannin (100 nmol/L, 60 min) or LY294002 (20 μmol/L, 30 min) followed by HG. (A) Translocation of PKC-β1 to the membrane, induced by HG for 30 min, was prevented by both inhibitors (n = 3; *P < 0.05 HG versus others). Actin served as the loading control for the cytosolic portion. (B) AP-1 activation was assessed by EMSA after HG treatment for 6 h. Both PI3K inhibitors prevented activation of this transcription factor (n = 4; *P < 0.05 HG versus others). (C) Similarly, TGF-β1 transcript upregulation after HG treatment for 24 h was prevented by both PI3K inhibitors, as assessed by Northern (n = 10; #P < 0.01 HG versus others). (D) TGF-β1 promoter activation was assessed by luciferase assay. Both PI3K inhibitors prevented promoter activation after HG treatment for 24 h (n = 5; #P < 0.01 HG versus others).