Fig. 5
From: Podocyte specific deletion of PKM2 ameliorates LPS-induced podocyte injury through beta-catenin
PKM2 deficiency ameliorates LPS-induced inflammation and apoptosis in cultured E11 podocytes. A Representative immunoblots (left panel) and bar graph quantitative assessment (right panel) of pIKKαS178/S180, IKKα, pIκBαS32, IκBα, pNF-κBp65S36, NF-κBp65, pJNK1/2T183/Y185, JNK, pP38T180/Y182, P38, and PKM2 in total cell lysates from 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. B Representative immunoblots (left panel) and bar graph quantitative assessment (right panel) of CHOP and cleaved-caspase 3 (C-Cas3) in total cell lysates from 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. C Caspase 3 activity in M2R and M2KD cells treated (LPS) or non-treated (Ctrl) with LPS for 24 h. **p < 0.01 indicate a significant difference between LPS-treated or non-treated cells. &&p < 0.01 indicate a significant difference between M2R and M2KD cells exposed to the same treatment. D Representative images of chromatin condensation in Hoechst-stained M2R and M2KD podocytes treated with LPS for 24 h. Scale bar: 100 μm. Images are representative of at least three independent experiments