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. 2021 Jan 11;162(4):bqab007. doi: 10.1210/endocr/bqab007

Figure 5.

Figure 5.

Effects of peroxisome proliferator-activated receptor (PPAR) agonist in Argonaute 2 (Ago2)-deficient primary hepatocytes. A, messenger RNA (mRNA) expression of Tfam-mitochondrial genes in liver-specific Ago2-deficiency (L-Ago2) wild-type (WT) (n = 6), and L-Ago2 knockout (KO) (n = 6) primary hepatocytes treated with or without 10-µM WY14643 (a PPARα agonist) for 24 hours. B, miR-27a and miR-27b expression in L-Ago2 WT (n = 6) and L-Ago2 KO (n = 6) primary hepatocytes treated with or without 10-µM WY14643 (PPARα agonist) for 24 hours. C, Oxygen consumption rate (OCR) of L-Ago2 WT (n = 12) and KO (n = 10–12) primary hepatocytes were measured in the presence or absence of a PPARα agonist (WY14643: 10 μM) pretreatment for 48 hours. D, PPARα target mRNA expression in L-Ago2 WT (n = 6) and L-Ago2 KO (n = 6) primary hepatocytes treated with or without 10-µM WY14643 (PPARα agonist) for 24 hours. Data are shown as mean± SEM. Statistical analyses were performed by 2-way analysis of variance for A, B, and D; and ordinary 1-way analysis of variance followed by Tukey post hoc test for C. *P less than or equal to .05, * P less than or equal to .01, *** P less than or equal to .001.