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. 2020 Aug 14;11(8):620. doi: 10.1038/s41419-020-02876-1

Fig. 2. Knockout of miR-382 contributes to reverse renal inflammation and fibrosis in mice.

Fig. 2

a Representative images of kidney sections from miR-382 WT or KO mice 14 d after the administering of 20 mg/kg AA (SAA group) with H&E and Masson staining, immunostaining for α-SMA as well as immunofluorescence for α-SMA, Vimentin and ZO-1. Scale bars, 100 or 50 μm. b Quantification of relative mRNA levels of miR-382 in mice kidney from miR-382 WT or KO mice 7, 14, and 28 days after the administering of 20 mg/kg AA; n = 6 per group. c–e Relative mRNA levels of IL-6, IL-10, and TNF-α in mice kidney tissues were examined in these groups. n = 6 per group. f–h Inhibition of miR-382 in mice reversed fibrotic manifestation of kidney significantly. Relative mRNA expression of Collagen I, Collagen III, and α-SMA in mice kidney tissues were examined between miR-382 WT and KO group 7 and 14 d following the administering of 20 mg/kg AA. n = 6 in each group. i–k Quantification of mean Fluorescence intensity for α-SMA, Vimentin, and ZO-1 between miR-382 WT and KO group 14 d following the administering of 20 mg/kg AA. We randomly choose five microscopical field per sections, n = 3 mice per group. l, n, o Representative and quantification immunoblot analysis of Fibronectin and Collagen IV in renal tissue from miR-382 WT or KO mice 14 d following 20 mg/kg AA treatment. GAPDH served as the standard; n = 6 in each group. m, p–s Representative and quantification immunoblot analysis of E-cadherin, N-cadherin Vimentin, and α-SMA in renal tissue from miR-382 WT or KO mice 14 d following 20 mg/kg AA treatment. GAPDH served as the standard; n = 6 in each group. *P < 0.05; **P < 0.01; ANOVA.