FIGURE 4.

miR‐422a suppressed proliferation and fibrosis of MCs by targeting IGF1R. A, Five genes were screened in MCs transfected with mimic‐miR‐422a. B, The expression level of miR‐422a was upregulated in MCs transfected with inhibitor‐miR‐422a. C, The protein expression level of IGF1R was increased by inhibitor‐miR‐422a and decreased by mimic‐miR‐422a. D, The direct binding sites between miR‐422a and IGF1R were presented. E, Luciferase reporter assay was performed to confirm the direct binding relationship between miR‐422a and IGF1R. F, Proliferating mesangial cells were labelled with EdU. Inhibitor‐miR‐422a enhanced the growth of MCs. G, Inhibitor‐miR‐422a enhanced the expression level of markers of fibrosis: p‐cadherin, ZO‐1 and TGF‐β1. H, and I, Efficiency of pcDNA3.1‐IGF1R were detected by qPCR and western blotting. J, and K, Overexpression of IGF1R enhanced the growth and fibrosis of MCs. L, The CCK8 assays indicated that the growth of MCs was promoted by inhibitor‐miR‐422a, but this promotion was eliminated when IGF1R was knocked down in MCs. M, Western blotting results showed that the expression level of p‐cadherin, ZO‐1 and TGF‐β1 was upregulated in MCs treated with inhibitor‐miR‐422a, but this promotion was restored when IGF1R was downregulated in MCs