Figure 5.

MicroRNA 122 (miR-122) contributes to liver-specific silencing of Oxct1 expression. (A) Time course of miR-122 expression in vivo during liver maturation as measured by qPCR. miR-122 increases with a linear trend, P = 0.01. Statistical significance of the difference between P42 and other time points was calculated by one-way ANOVA with a Dunnett post-hoc test. (B) Treatment of in vitro differentiated BMEL cells with antagomiR-122 (α-miR-122) or a mutated antagomiR (α-miR-122 mut) control. Changes in miR-122 expression (left) and Oxct1 expression (right) were measured by Q-PCR. MiR-122 expression decreases sixfold by treatment with antagomiR-122 (α-miR-122). A mutated antagomiR (α-miR-122 mut) control did not significantly influence miR-122 expression. Oxct1 expression is increased by miR-122 knockdown with antagomiR-122, indicating that miR-122 inhibits Oxct1 expression. A mutated antagomiR did not significantly alter Oxct1 expression. Data are means ± SEM of three individual experiments. (C) Oxct1 RNA and protein expression in livers at E15.5 of wild-type versus liver-specific miR-122 overexpressing transgenic mice. A 1.7 ± 0.07-fold overexpression of miR-122 (mean ± SEM; n = 4 [wild-type] and n = 6 [transgenic]) was associated with a significant (t-test, P < 0.05) repression of Oxct1 RNA and protein, as determined by Q-RT-PCR (n = 4 or 6 for wild-type or transgenic, respectively) and Western blotting (n = 3). *P < 0.05; **P < 0.01; ***P < 0.001.