Fig. 2

PKM2 podocyte deletion ameliorates LPS induced proteinuria and kidney injury. A Representative immunoblots (left panel) of PKM2, PKM1, PKM1/2, and β-Actin in whole kidney lysates from wild type (Ctrl) and podocyte PKM2 knockout mice (KO). mRNA levels (right panel) of Pkm2 in total kidney lysates of Ctrl and KO mice (n = 6 group). B Representative immunoblots (left panel) of PKM2, PKM1, PKM1/2, and β-Actin in primary podocytes isolated from Ctrl and KO mice. The right panel is the mRNA level of Pkm2 and Pkm1 C in primary podocytes (n = 12; 4 animals/lane). D Body weights, E kidney weights, and F kidney to body weight ratio of wild type (Ctrl) and podocyte PKM2 knockout mice (KO) mice, under PBS and LPS treated states. Assessment of G total urinary proteins levels, H serum albumin levels, I urine albumin levels, J albumin to creatinine ratios (ACR), and K blood urea nitrogen (BUN) levels of Ctrl and KO mice after PBS and LPS injection (n = 6–12 per group). L PAS staining of kidney sections in Ctrl and KO mice under PBS and LPS conditions; the arrow is pointing to the expansion of Bowman space in response to LPS treatment. Scale bar = 50 μM. M Immunofluorescence of Nephrin (green), PKM2 (red), and nuclear DNA using DAPI (blue) in kidney sections obtained from both genotypes injected with PBS or LPS. Scale bar = 50 μM. In D–K, *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