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Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis
Cell Biology
Volume 4, Issue 1, January 2016, Pages: 1-8
Received: Mar. 18, 2016; Accepted: Mar. 28, 2016; Published: Apr. 13, 2016
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Authors
Xiaofang Zhao, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Fuli Yao, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Chunyan Zhang, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Ying Cheng, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Bin Xiao, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Yuxiao Li, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Chunyan Duan, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Youping Liu, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Hong Li, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
Rongyang Dai, Department of Biochemistry and Molecular Biology, Southwest Medical University, Luzhou, Sichuan, China
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Abstract
Saturated free fatty acids-induced hepatocyte lipoapoptosis plays a pivotal role in non-alcoholic steatohepatitis. The activation of endoplasmic reticulum (ER) stress is involved in hepatocyte lipoapoptosis induced by the saturated free fatty acid palmitate (PA). However, the underlying mechanisms of the role of ER stress in hepatocyte lipoapoptosis remain largely unclear. In this study, we showed that PA and tunicamycin (Tun), a classic ER stress inducer, resulted in differential activation of ER stress pathways. Our data revealed that PA induced chronic and persistent ER stress response, but Tun induced acute and transient ER stress response. Compared with Tun treatment, PA induced much lower glucose-regulated protein 78 (GRP78), a central regulator of ER homeostasis, accumulation. It is noteworthy that GRP78 over-expression not only inhibited PA-induced ER stress but also decreased PA-induced apoptosis. Taken together, our data suggest that the differential activation of ER stress signal plays an important role in PA-induced hepatocyte lipoapoptosis. More detailed studies on the mechanisms of PA in repressing the accumulation of GRP78 will contribute to the understanding of molecular mechanisms of lipoapoptosis.
Keywords
ER Stress, Palmitate, Hepatocyte Lipoapoptosis, GRP78
To cite this article
Xiaofang Zhao, Fuli Yao, Chunyan Zhang, Ying Cheng, Bin Xiao, Yuxiao Li, Chunyan Duan, Youping Liu, Hong Li, Rongyang Dai, Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis, Cell Biology. Vol. 4, No. 1, 2016, pp. 1-8. doi: 10.11648/j.cb.20160401.11
Copyright
Copyright © 2016 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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