Long Noncoding RNA MALAT1 Acts as a Competing Endogenous RNA to Regulate TGF-β2 Induced Epithelial-Mesenchymal Transition of Lens Epithelial Cells by a MicroRNA-26a-Dependent Mechanism
Figure 3
Smad4 is a target of miR-26a in primary HLECs. (a) The levels of miR-26a were detected by qRT-PCR. P < 0.05 compared with normal-attached LECs or nuclear cataracts. (b) Smad4 protein levels in primary HLECs were detected by Western blot analysis. The primary HLECs were treated with TGF-β2 (5 ng/ml) for 48 h before incubation with miR-26a mimics or miR-26a mimics negative control for 6 h. (c) Smad4 protein levels in primary HLECs were detected by Western blot analysis. The primary HLECs were treated with TGF-β2 (5 ng/ml) for 48 h before incubation with anti-miR-26a or anti-miR-26a negative control for 6 h. (d) The levels of Smad4 mRNA were detected by qRT-PCR. P < 0.05 compared with normal or TGF-β2 group. (e) The luciferase reporter assays identified that miR-26a directly targets Smad4 in HLECs. P < 0.05 compared with miR-26a mimics control group. All of data are presented as the mean± SE of six independent experiments.