Fig. 3: EZH2 conditional knockout protects against renal dysfunction, suppresses renal fibrosis and loss of TEC transporters in FA induced AKI-to-CKD transition mouse model.
The mice in FA model were injected with a single dose of folic acid (250 mg/kg, dissolved in 300 mM NaHCO3, i.p.), while the control group was injected with an identical voluminal vehicle (300 mM NaHCO3, i.p.) for 4 weeks. A Photograph showed the size, color, and texture of kidney in each group. B Serum creatinine of the mice in different groups. C Blood urea nitrogen (BUN) of the mice in different groups. D Photomicrographs showed the PAS staining of the kidneys. E Morphologic change of tubular injury was scored on the basis of PAS staining described in the Method section. F Photomicrographs showed the Masson’s trichrome staining of the kidneys. G The graph showed the positive areas (blue) of Masson’s trichrome staining. H Kidney tissue lysates from FA mice were subjected to immunoblotting analysis with specific antibodies against EZH2, H3K27me3, Histone H3 and GAPDH. I, J Expression levels of EZH2 and H3K27me3 in different groups were quantified by densitometry and normalized with GAPDH and Histone H3 respectively. K Kidney tissue lysates from FA mice were subjected to immunoblotting analysis with specific antibodies against α-SMA, Collagen I, E-cadherin, and GAPDH. L–N Expression levels of α-SMA, Collagen I, E-cadherin in different groups were quantified by densitometry and normalized with GAPDH. (O) Kidney tissue lysates from FA mice were subjected to immunoblotting analysis with specific antibodies against OAT1, AQP1, ATPase and GAPDH. P–R Expression levels of OAT1, AQP1, and ATPase in different groups were quantified by densitometry and normalized with GAPDH. 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.
