Fig. 3
From: Podocyte specific deletion of PKM2 ameliorates LPS-induced podocyte injury through beta-catenin
Podocyte specific deletion of PKM2 attenuates LPS-Induced inflammation and apoptosis in Vivo. A Representative immunoblots (left panel) and bar graph quantitative assessment (right panel) of major signal transduction molecules involved in the NF-κB (pIKKαS178/S180, IKKα, pIκBαS32, IκBα, pNF-κBp65S36, NF-κBp65), MAPK (pJNK1/2T183/Y185, JNK, pP38T180/Y182, P38) signaling pathways, and β-Actin as a loading control in whole kidney lysates of control (Ctrl) and podocyte PKM2 knockout mice (KO) mice harvested 24 h after PBS or LPS injection (n ≥ 6/group). *p < 0.05, **p < 0.01 indicate a significant difference between PBS- and LPS-injected mice. &p < 0.05, &&p < 0.01 indicate a significant difference between Ctrl and KO mice. B Representative immunoblots (left panel) and bar graph quantification (right panel) of apoptotic markers: Caspase 12, 7, and 3, their cleaved forms, and CHOP in whole kidney lysates of control (Ctrl) and podocyte PKM2 knockout mice (KO) mice harvested 24 h after PBS or LPS injection (n ≥ 6/group). *p < 0.05, **p < 0.01 indicate a significant difference between PBS- and LPS-injected mice. &p < 0.05, &&p < 0.01 indicate a significant difference between Ctrl and KO mice