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. 2021 Feb 3;13(4):4881–4894. doi: 10.18632/aging.202617

Figure 4.

Figure 4

miR-141-3p induces mitochondrial dysfunction and impairs muscle differentiation through downregulation of Fkbp5/Fibin. (A–D) Mitochondrial respiration was measured in miR-141-3p overexpressed (A) or silenced (C) C2C12 cells. Average OCR values were indicated in miR-141-3p overexpressed (B) or silenced (D) C2C12 cells. (E, F) Mitochondrial respiration (E) and average OCR value (F) were measured in Fkbp5 knockdown C2C12 cells. (G, H) Mitochondrial respiration (G) and average OCR value (H) were measured in Fibin knockdown C2C12 cells. (I–L) C2C12 cells were treated with miR-141-3p mimic or miR-141-3p inhibitor and induced to differentiate. The expression of MHC was analyzed by immunostaining (I–K). Cells were stained with anti-MHC (green) and DAPI (blue) for nuclei detection. Fusion index of miR-141-3p mimic (J) or miR-141-3p inhibitor (L) was calculated. Data are means ± SEM. *P<0.05, **P<0.01; unpaired two-tailed Student’s t-test. (M) Fkbp5 or Fibin silenced C2C12 cells were differentiated and immunostaining was conducted to measure the expression of MHC. (N) Fusion index of Fkbp5 or Fibin silenced C2C12 cells. Data are means ± SD.**P<0.01 vs si_Scr; one-way ANOVA with post hoc Dunnett’s multiple comparison test.