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miR-222 targets ACOX1, promotes triglyceride accumulation in hepatocytes
Jing-Jie Wang1, Yi-Tong Zhang1, Yu Jen Tseng1
1Department of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai 200040, China.
Background:
Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases. However, the exact pathogenesis of NAFLD remains to be elucidated. Despite the association with tumors and cardiovascular diseases, the role of miR-222 in NAFLD remains unclear. The present study was to investigate the role of miR-222 in NAFLD.
Methods:
Wild-type C57BL/6 mice were fed a high-fat diet for 12 weeks to induce NAFLD. Normal human liver cell line (L02) was cultured with free fatty acid (FFA)-containing medium to stimulate cell steatosis. The mRNA levels of miR-222 and acyl Coenzyme A xidase 1 (ACOX1) were detected by quantitative-PCR (Q-PCR). The prediction of ACOX1 as the target gene for miR-222 was conducted via TargetScan. The overexpression or inhibition of miR-222 was mediated by miR-222 mimics or antagomir, and intracellular triglyceride levels were measured using a triglyceride kit. Luciferase reporter assays verified ACOX1 as the target gene for miR-222.
Results:
miR-222 was significantly elevated in both the in vivo and in vitro NAFLD models. Overexpression of miR-222 significantly increased triglyceride content in the L02 cells, while inhibition of miR-222 expression restricted the accumulation of triglyceride. Overexpression of miR-222 significantly inhibited ACOX1 expression. Transient transfection assays verified that ACOX1 3'-UTR luciferase reporter activity could be inhibited by miR-222 overexpression.
Conclusions:
The present study suggested that miR-222 promotes the accumulation of triglycerides by inhibiting ACOX1.
Insights
MicroRNA-222 (miR-222) promotes non-alcoholic fatty liver disease (NAFLD) by increasing triglyceride accumulation. Inhibiting miR-222 may offer a therapeutic strategy for NAFLD by reducing fat buildup.
Area of Science:
- Hepatology
- Molecular Biology
- Biochemistry
Background:
- Non-alcoholic fatty liver disease (NAFLD) is a widespread condition with unclear pathogenesis.
- The specific role of microRNA-222 (miR-222) in NAFLD development is not well understood.
- Investigating miR-222's function is crucial given NAFLD's association with other serious health issues.
Purpose of the Study:
- To elucidate the role of miR-222 in the pathogenesis of NAFLD.
- To determine if miR-222 influences triglyceride accumulation in liver cells.
- To identify the molecular targets of miR-222 in the context of NAFLD.
Main Methods:
- NAFLD was induced in mice using a high-fat diet and in L02 liver cells with free fatty acids.
- Quantitative PCR (Q-PCR) was used to measure miR-222 and ACOX1 mRNA levels.
- miR-222 mimics/antagomirs and luciferase reporter assays were employed to assess gene regulation and function.
Main Results:
- miR-222 levels were significantly elevated in both in vivo and in vitro NAFLD models.
- Overexpression of miR-222 increased intracellular triglyceride content, while inhibition reduced it.
- miR-222 was confirmed to target and inhibit the expression of acyl Coenzyme A oxidase 1 (ACOX1).
Conclusions:
- miR-222 plays a pro-steatotic role in NAFLD.
- The mechanism involves miR-222 promoting triglyceride accumulation by suppressing ACOX1.
- Targeting miR-222 could be a potential therapeutic approach for managing NAFLD.
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