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. 2015 Nov 10;5:16422. doi: 10.1038/srep16422

Figure 6. miR-128 regulates apoptosis through prohibitin.

Figure 6

(A) Knockdown of miR-128 could attenuate apoptosis. Cardiomyocytes were transfected with miR-128 antagomir or the antagomir negative control (Antagomir-NC). 24 hours after transfection, cells were treated with 100 μM hydrogen peroxide. Apoptosis was analyzed by the TUNEL assay. *p < 0.05 vs hydrogen peroxide alone. (B) Constructs of prohibitin with wild type 3′UTR (prohibitin-wt 3′UTR) or mutated 3′UTR (prohibitin-m 3′UTR, the mutations are underlined). (C) miR-128 significantly reduces the expression levels of prohibitin with wild type 3′UTR but not with mutated 3′UTR. Cardiomyocytes were infected with the adenoviral construct of miR-128, along with the construct of prohibitin-wt 3′UTR or prohibitin-m 3′UTR. 24 h after infection, cells were treated with 100 μM hydrogen peroxide. Prohibitin levels were analyzed by immunoblotting and the total amount of β-actin served as internal control. (D) Prohibitin with mutated 3′UTR can more efficiently inhibit apoptosis than that with wild type 3′UTR in the presence of miR-128. Cardiomyocytes were treated as described for (C). Apoptosis was analyzed by the TUNEL assay. *p < 0.05.