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. 2020 Jan 1;10(2):553–566. doi: 10.7150/thno.37181

Figure 3.

Figure 3

miR-153-3p regulates Mfn1 expression. (A) Cardiomyocytes were exposed to ISO and harvested at indicated times. The expression level of miR-153-3p was analyzed by qRT-PCR. *p < 0.05 vs 0 h. (B) Analysis of Mfn1 3'UTR region for the potential binding site of miR-153-3p. (C) Knockdown of miR-153-3p did not affect the level of Mfn1 mRNA. Cardiomyocytes were transfected with antagomir of miR-153-3p (anta-153-3p) or antagomir-negative control (anta-NC) and the level of Mfn1 mRNA was detected by qRT-PCR. (D) Knockdown of miR-153-3p increases Mfn1 protein level. Cardiomyocytes were treated as described in (C). The level of Mfn1 protein was detected by immunoblot. (E) Cardiomyocytes were transfected with miR-153-3p mimic (mimic-153-3p) or its negative control (mimic-NC), and Mfn1 protein level was detected by immunoblot. (F) Cardiomyocytes transfected with anta-153-3p or anta-NC were exposed to ISO and the level of Mfn1 protein was detected by immunoblot. (G) miR-153-3p inhibits translation of Mfn1 mRNA. HEK293 cells were cotransfected with the luciferase construct carrying wild-type Mfn1-3'UTR (Mfn1-3'UTR-wt) or mutated Mfn1-3'UTR (Mfn1-3'UTR-mut) and mimic-153-3p or mimic-NC and cells were harvested for the measurement of luciferase activity. *p < 0.05.