Fig. 8
- ID
- ZDB-FIG-180807-15
- Publication
- Lai et al., 2018 - Liver-directed microRNA-7a depletion induces nonalcoholic fatty liver disease by stabilizing YY1-mediated lipogenic pathways in zebrafish
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PPAR-? antagonists and miR-7a mimic treatment ameliorate NAFLD and NASH phenotypes in hC7aSP1 fed with LFD. (A) Steatotic analyses of 9?dpf WT and hC7aSP1r larvae. Embryos without injection (NI) and those injected with 200?pg PPAR-? mRNA, 150?pg C/EBP-? mRNA, and 200?pg CHOP-10 mRNA were analyzed at the embryonic stage of 7?dpf. (B) Quantification of hepatic steatosis of WT and hC7aSP1 is shown in (A). The total number (N) of larvae in each group is indicated. (C) Western blot analyses of CHOP-10 ectopic efficiency. hC7aSP1 larvae and WT embryos without injection (NI) and those injected with 200?pg CHOP-10 mRNA were harvested at 9?dpf. ?-Actin was used as the loading control. (D) Gross anatomy of liver and frozen liver section ORO staining in hC7aSP1 adults treated with miR-7a mimic, Gw9962, ASX, miR-7a mimic?+?GW9962, and miR-7a mimic?+?GW9962 (rescued hC7aSP1). (E) qRT-PCR analysis of selected lipogenic genes in the livers of rescued hC7aSP1. (F) qRT-PCR analysis of selected NASH-like genes in the livers of rescued hC7aSP1. Levels of mRNA were normalized to ?-actin and expressed as fold of values in the WT control. **p?<?0.01; *p?<?0.05. |