Hepatic HuR modulates lipid homeostasis in response to high-fat diet

Zhuojun Zhang, Chen Zong, Mingyang Jiang, Han Hu, Xiaolei Cheng, Juhua Ni, Xia Yi, Bin Jiang, Feng Tian, Ming-Wen Chang, Wen Su, Lijun Zhu, Jinfan Li, Xueping Xiang, Congxiu Miao, Myriam Gorospe, Rafael Cabo, Yali Dou, Zhenyu Ju, Jichun Yang, Changtao Jiang, Zhongzhou Yang () and Wengong Wang ()
Additional contact information
Zhuojun Zhang: Peking University Health Science Center
Chen Zong: Peking University Health Science Center
Mingyang Jiang: Nanjing University
Han Hu: Peking University Health Science Center
Xiaolei Cheng: Peking University Health Science Center
Juhua Ni: Peking University Health Science Center
Xia Yi: Peking University Health Science Center
Bin Jiang: Peking University Health Science Center
Feng Tian: Peking University Health Science Center
Ming-Wen Chang: National Institutes of Health
Wen Su: Shenzhen University Health Science Center
Lijun Zhu: Zhejiang University
Jinfan Li: Zhejiang University
Xueping Xiang: Zhejiang University
Congxiu Miao: Changzhi Medical College
Myriam Gorospe: National Institutes of Health
Rafael Cabo: National Institutes of Health
Yali Dou: University of Michigan
Zhenyu Ju: Jinan University
Jichun Yang: Peking University Health Science Center
Changtao Jiang: Peking University Health Science Center
Zhongzhou Yang: Nanjing University
Wengong Wang: Peking University Health Science Center

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract Lipid transport and ATP synthesis are critical for the progression of non-alcoholic fatty liver disease (NAFLD), but the underlying mechanisms are largely unknown. Here, we report that the RNA-binding protein HuR (ELAVL1) forms complexes with NAFLD-relevant transcripts. It associates with intron 24 of Apob pre-mRNA, with the 3′UTR of Uqcrb, and with the 5′UTR of Ndufb6 mRNA, thereby regulating the splicing of Apob mRNA and the translation of UQCRB and NDUFB6. Hepatocyte-specific HuR knockout reduces the expression of APOB, UQCRB, and NDUFB6 in mice, reducing liver lipid transport and ATP synthesis, and aggravating high-fat diet (HFD)-induced NAFLD. Adenovirus-mediated re-expression of HuR in hepatocytes rescues the effect of HuR knockout in HFD-induced NAFLD. Our findings highlight a critical role of HuR in regulating lipid transport and ATP synthesis.

Date: 2020
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DOI: 10.1038/s41467-020-16918-x

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