Abstract
Alcoholic liver disease (ALD) is a global liver disease which characterized by liver inflammation, fatty liver, alcoholic hepatitis, or liver cirrhosis. Alcohol abuse is one of the main reasons for liver disease. Alcoholic fatty liver (AFL) disease is the early stage of ALD and associated with the excessive lipids accumulation in hepatocytes as well as oxidative stress. MicroRNA-203 (miR-203) is known to suppress the proliferation and metastasis of hepatocellular carcinoma, but the role in the progression of alcoholic liver disease is not clear and is warranted for further investigation. In the present study, we have found the expression of miR-203 is down-regulated in Gao-Binge alcoholic mice model and ethanol-induced AML-12 cell lines in vitro. Furthermore, over-expression of miR-203 decrease the lipids accumulation in liver and ethanol-induced AML-12 cells. Mechanistically, we identified that Lipin1 is a key regulator of hepatic lipid metabolism, and acts as a downstream target for miR-203. In summary, our results suggested that over-expression of miR-203 inhibited the liver lipids accumulation and the progression of AFL by targeting Lipin1.
Highlights
Alcoholic liver disease (ALD) is one of the most common liver diseases in the world and it becomes a major cause of affecting the morbidity and mortality worldwide (Ramaiah et al, 2004)
We proved that miR-203 could regulate the biological progression of ALD via directly targeting Lipin1 expression
ALD model was constructed by reference the National Institute on Alcohol Abuse and Alcoholism (NIAAA), more details can be found in the article (Wu et al, 2016)
Summary
Alcoholic liver disease (ALD) is one of the most common liver diseases in the world and it becomes a major cause of affecting the morbidity and mortality worldwide (Ramaiah et al, 2004). Metabolism of alcohol triggers activation of the innate immune cells in the liver, increases the generation of cellular NADH. Metabolism of alcohol can impair oxidation and tricarboxylic acid cycle activity. This leads to a lot of free fatty acid overload in turn, increased synthesis and secretion of triacylglycerol (TG), very low-density lipoprotein (VLDL), which contributes to the development and pathogenesis of ALD. It has been said that patients who consume alcohol chronically develop steatosis due in part to alterations in lipid metabolism (Crabb and Liangpunsakul, 2006) and without treatment may develop to advanced stages of ALD that include liver fibrosis and liver cirrhosis (MacSween and Burt, 1986)
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