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. 2021 Jan 7;70(3):710–719. doi: 10.2337/db20-0181

Figure 2.

Figure 2

Elevated miR-378a induces mitochondrial and ER stress via mediation of PPARα signaling. A: AML12 cells were transfected with miR-378a or scrambled (Scram) miRNA (10 nmol/L) as control for 60 h and subjected to protein extraction. Mitochondrial and ER stress markers HSP60, Grp78, and eIF2α-p as well as total eIF2α and β-actin were determined by immunoblotting analysis. B: Oxygen consumption rate (OCR) was determined in McA cells transfected with miR-378a or mock (GFP) for 12 h followed by treatment with PPARα agonist WY14,643 (30 μmol/L) or vehicle (Veh) (DMSO) for an additional 24 h using Seahorse (FX24) analysis in the presence of 1 μmol/L oligomycin (Oligo), 1 μmol/L carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP), and 0.5 μmol/L rotenone (Rot). C: Protein expression of PPARα and mitochondrial and ER stress markers HSP60, Grp78, JNK-p, p-NFκB-p65, and eIF2α-p in the livers of WT or miR-378a-KO mice fed a high-fructose diet for 4 weeks were determined by immunoblotting analysis (n = 5/group). For cell treatment, two independent experiments were performed in triplicate. Data are mean ± SD. The two-tailed Student t test was used for statistical analyses of two-group comparisons. *P < 0.05 vs. controls. Fruc, fructose.