Journal
JOURNAL OF MOLECULAR MEDICINE-JMM
Volume 93, Issue 9, Pages 1045-1055Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00109-015-1282-2
Keywords
miR-26a; Autophagy; Hepatic steatosis; Mitogen-activated protein kinases; Ethanol binge
Funding
- National Natural Science Foundation of China [81372621, 81441121]
- American Cancer Society [RSG-11-132-01-CCE]
- NCI [1R01-CA139158]
- National Health and Family Planning Commission [2015112271]
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Autophagy is a process for the turnover of intracellular organelles and molecules during stress responses. microRNAs (miRNAs) are small, non-coding endogenous RNAs that may regulate almost every cellular process. However, the roles of miRNAs in autophagy are still poorly understood. In this study, we show that miR-26a enhances autophagy in both culture cells and the mouse liver. Hepatic overexpression of miR-26a in mice alleviated ethanol-induced hepatic steatosis and liver injury. Overexpression of miR-26a increased the expression of the autophagy mediator Beclin-1, which is regulated by mitogen-activated protein kinases (MAPKs). We identified DUSP4 and DUSP5, two MAPKs inhibitors, as direct targets of miR-26a. We further demonstrated that miR-26a targeted the 3'-UTRs of several other negative regulators of autophagy. Our results thus identify a novel miRNA-mediated mechanism that enhances cytoprotective autophagy in the liver. aEuro cent miR-26a enhances autophagy in liver cells. aEuro cent Hepatic overexpression of miR-26a in mice alleviates ethanol-induced liver injury. aEuro cent Overexpression of miR-26a increases the expression of autophagy mediator Beclin-1. aEuro cent DUSP4 and DUSP5, two MAPKs inhibitors, were identified as direct targets of miR-26a.
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