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Beyond PI3K, Akt is involved in TNF-α stimulation of MCP-1 in podocytes. The marked increase in MCP-1 production due to 10 ng/ml TNF-α for 6 h was significantly blunted by pretreatment with 750 nM Akt inhibitor IV. In the absence of TNF-α, Akt inhibitor IV also seemed to reduce the expression of MCP-1 at baseline, but Akt inhibitor IV vs. control was not statistically significant. p values are as shown (n = 3).
