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Impact of miR-140 Deficiency on Non-Alcoholic Fatty Liver Disease
Benjamin Wolfson1, Pang-Kuo Lo1, Yuan Yao1
1Department of Biochemistry and Molecular Biology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, 21201, USA.
Scope:
We have previously shown that loss of miR-140 has a pro-fibrotic effect in the mammary gland. This study aims to investigate whether miR-140 loss and obesity act synergistically to promote non-alcoholic fatty liver disease (NAFLD), and to identify the underlying mechanisms.
Methods And Results:
Liver tissues were isolated from lean-fat-diet and high-fat-diet fed wild-type and miR-140 knockout mice. Using molecular staining and immunohistochemistry techniques, increased development of NAFLD and fibrotic indicators in miR-140 knockout mice were identified. Utilizing an in vitro model system, miR-140 was demonstrated to target TLR-4, and miR-140 overexpression was shown to be sufficient to inhibit palmitic acid signaling through the TLR-4/NFκB pathway.
Conclusion:
These findings demonstrate that loss of miR-140 results in increased expression of TLR-4, sensitizing cells to palmitic acid signaling and in increased inflammatory activity through the TLR4/NFκB pathway. This signaling axis promotes NAFLD development in a high-fat diet context and indicates the potential utility of miR-140 rescue as a therapeutic strategy in NAFLD.
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