Role of glycoprotein 78 and cidec in hepatic steatosis

Li,Jie; Liu,Guocai; Zhang,Feng; Zhang,Zhiwen; Xu,Yuqiao; Li,Qing

doi:10.3892/mmr.2017.6834

Role of glycoprotein 78 and cidec in hepatic steatosis

Authors:
- Jie Li
- Guocai Liu
- Feng Zhang
- Zhiwen Zhang
- Yuqiao Xu
- Qing Li
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Affiliations: State Key Laboratory of Cancer Biology, Department of Pathology, Xijing Hospital, Basic Medical College, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China, The Third Department of Internal Medicine, The 273 Hospital of Chinese PLA, Korla, Xinjiang 84100, P.R. China
Published online on: June 21, 2017 https://doi.org/10.3892/mmr.2017.6834
Pages: 1871-1877
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Hepatic glycoprotein (gp78), a membrane-anchored E3 ubiquitin ligase, has been reported to be involved in regulating lipid and energy metabolism in animals, and cell death‑inducing DFFA‑like effector c (cidec) has emerged as an important regulator of metabolism, which has been implicated in the process of fat differentiation. Nonalcoholic fatty liver disease is a metabolic disorder associated with hepatic steatosis. In the present study, to investigate the role of gp78 and cidec in hepatic steatosis, an in vitro cell culture model of hepatic steatosis was established, using the AML12 mouse hepatocyte cell line to assess the protein expression of gp78. The results of Oil Red O staining, phase contrast microscopy and triglyceride content detection experiments indicated that the overexpression of gp78 induced lipid accumulation, whereas gp78‑knockdown led to a reduction in lipid accumulation in the AML12 cells. The increased expression of gp78 was associated with steatosis. The expression of cidec was consistent with gp78, and the colocalization of gp78 and cidec was observed on the surface of lipid droplets using immunofluorescence analysis. Furthermore, an interaction between gp78 and cidec was detected using coimmunoprecipitation analysis, and this interaction promoted lipid accumulation. Based on these data, it was hypothesized that gp78 is a regulator of hepatic steatosis, and that it may be a putative molecular mediator in metabolic diseases.

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