Fig. 4
From: Podocyte specific deletion of PKM2 ameliorates LPS-induced podocyte injury through beta-catenin
PKM2 deficiency in cultured E11 podocytes alleviates LPS-induced nephrin loss. A Representative immunoblots (left panel) and bar graph quantitative assessment (right panel) of PKM2, PKM1, and PKM1/2 levels in undifferentiated (day 1; D1) and differentiated (D15) E11 murine podocytes infected with lentivirus particles carrying scramble-shRNA (SCR), shRNA targeting PKM2 (M2KD) or an open reading frame of the human DNA (M2R). β-Actin was used as a loading control. *p < 0.05, **p < 0.01 indicate a significant difference between differentiated and undifferentiated cells. #p < 0.05, ##p < 0.01 indicate a significant difference between the indicated cell and control E11 cells exposed to the same treatment. B Representative immunoblots (left panel) and bar graph quantitative assessment (right panel) of pPKM2Y105, pPKM2S37, PKM2, PKM1, PKM1/2, and Nephrin in differentiated M2R and M2KD podocytes treated with LPS for the indicated durations. β-Actin was used as a loading control. Data is representative of at least three independent experiments. *p < 0.05, **p < 0.01 indicate a significant difference between LPS-treated or non-treated cells. &p < 0.05, &&p < 0.01 indicate a significant difference between M2R and M2KD cells exposed to the same treatment