Fig. 8: EZH2 conditional knockout inhibits M2 macrophage polarization through STAT6 and PI3K/AKT pathways in I/R or FA induced AKI-to-CKD transition mice models.

A Photomicrographs showed the immunofluorescent staining of CD163 in different groups. B Kidney tissue lysates from I/R mice were prepared and subjected to immunoblotting analysis with antibodies against CD163, Arginase-1, MMP9, and GAPDH. C–E Expression levels of CD163, Arginase-1, MMP9 in different groups were quantified by densitometry and normalized with GAPDH. F Kidney tissue lysates from I/R mice were prepared and subjected to immunoblotting analysis with antibodies against p-STAT6, STAT6, p-PI3K, PI3K, p-AKT, AKT, and GAPDH. G–I Expression levels of p-STAT6, p-PI3K, and p-AKT were quantified by densitometry and normalized with STAT6, PI3K, and AKT. J Kidney tissue lysates from FA mice were prepared and subjected to immunoblotting analysis with antibodies against CD163, Arginase-1, MMP9, and GAPDH. K Kidney tissue lysates from FA mice were prepared and subjected to immunoblotting analysis with antibodies against p-STAT6, STAT6, p-PI3K, PI3K, p-AKT, AKT, and GAPDH. L–N Expression levels of p-STAT6, p-PI3K, and p-AKT were quantified by densitometry and normalized with STAT6, PI3K, and AKT. O The role and mechanisms of EZH2 in AKI-to-CKD transition. Data were expressed as means ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. N.S., statistically not significant, with the comparisons labeled. All scale bars = 50 μm.