Fig. 5: miR-181c-5p leads to hiPSCs differentiation into IPCs through negative regulation of smad7 and TGIF2. | Cell Death & Disease

Fig. 5: miR-181c-5p leads to hiPSCs differentiation into IPCs through negative regulation of smad7 and TGIF2.

From: microRNA-181c-5p promotes the formation of insulin-producing cells from human induced pluripotent stem cells by targeting smad7 and TGIF2

Fig. 5

a, b The dynamic expression levels of smad7 and TGIF2 at the mRNA and protein levels were quantified by real-time PCR and western blot, respectively. hiPSCs were infected with miR-181c-5p or negative control lentivirus and then induced into IPCs. The data are expressed as the mean ± SD of three independent experiments (n = 7). *p ≤ 0.05, **p ≤ 0.001, relative to the hiPSCs control. c Endogenous expression levels of smad7, TGIF2, and phosphorylation-smad2/3 were analyzed by western blot. d The effect of phosphorylation-smad2 and phosphorylation-smad3 inhibitors on differentiated hiPSCs was evaluated by flow cytometry. Inhibitor: S1, inhibitors only used in stage 1; Inhibitor: S2-S4, inhibitors used from stage 2 to stage 4; Inhibitor: S5, inhibitors only used in stage 5. LY2109761, phosphorylation-smad2 inhibitor. SIS3 HCl, phosphorylation-smad3 inhibitor. e Proposed mechanism for the regulation of hiPSCs differentiation into IPCs by microRNA-181c-5p.

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