Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis

Xiaofang Zhao; Fuli Yao; Chunyan Zhang; Ying Cheng; Bin Xiao; Yuxiao Li; Chunyan Duan; Youping Liu; Hong Li; Rongyang Dai

doi:doi:10.11648/j.cb.20160401.11

Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis

Xiaofang Zhao, Fuli Yao, Chunyan Zhang, Ying Cheng, Bin Xiao, Yuxiao Li, Chunyan Duan, Youping Liu, Hong Li, Rongyang Dai

Published in Cell Biology (Volume 4, Issue 1)

Received: 18 March 2016 Accepted: 28 March 2016 Published: 13 April 2016

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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.

Published in	Cell Biology (Volume 4, Issue 1)
DOI	10.11648/j.cb.20160401.11
Page(s)	1-8
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

ER Stress, Palmitate, Hepatocyte Lipoapoptosis, GRP78

References

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APA Style

Xiaofang Zhao, Fuli Yao, Chunyan Zhang, Ying Cheng, Bin Xiao, et al. (2016). Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis. Cell Biology, 4(1), 1-8. https://doi.org/10.11648/j.cb.20160401.11

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ACS Style

Xiaofang Zhao; Fuli Yao; Chunyan Zhang; Ying Cheng; Bin Xiao, et al. Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis. Cell Biol. 2016, 4(1), 1-8. doi: 10.11648/j.cb.20160401.11

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AMA Style

Xiaofang Zhao, Fuli Yao, Chunyan Zhang, Ying Cheng, Bin Xiao, et al. Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis. Cell Biol. 2016;4(1):1-8. doi: 10.11648/j.cb.20160401.11

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@article{10.11648/j.cb.20160401.11,
  author = {Xiaofang Zhao and Fuli Yao and Chunyan Zhang and Ying Cheng and Bin Xiao and Yuxiao Li and Chunyan Duan and Youping Liu and Hong Li and Rongyang Dai},
  title = {Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis},
  journal = {Cell Biology},
  volume = {4},
  number = {1},
  pages = {1-8},
  doi = {10.11648/j.cb.20160401.11},
  url = {https://doi.org/10.11648/j.cb.20160401.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20160401.11},
  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.},
 year = {2016}
}

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TY  - JOUR
T1  - Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis
AU  - Xiaofang Zhao
AU  - Fuli Yao
AU  - Chunyan Zhang
AU  - Ying Cheng
AU  - Bin Xiao
AU  - Yuxiao Li
AU  - Chunyan Duan
AU  - Youping Liu
AU  - Hong Li
AU  - Rongyang Dai
Y1  - 2016/04/13
PY  - 2016
N1  - https://doi.org/10.11648/j.cb.20160401.11
DO  - 10.11648/j.cb.20160401.11
T2  - Cell Biology
JF  - Cell Biology
JO  - Cell Biology
SP  - 1
EP  - 8
PB  - Science Publishing Group
SN  - 2330-0183
UR  - https://doi.org/10.11648/j.cb.20160401.11
AB  - 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.
VL  - 4
IS  - 1
ER  -

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Author Information

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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APA Style

Xiaofang Zhao, Fuli Yao, Chunyan Zhang, Ying Cheng, Bin Xiao, et al. (2016). Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis. Cell Biology, 4(1), 1-8. https://doi.org/10.11648/j.cb.20160401.11

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ACS Style

Xiaofang Zhao; Fuli Yao; Chunyan Zhang; Ying Cheng; Bin Xiao, et al. Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis. Cell Biol. 2016, 4(1), 1-8. doi: 10.11648/j.cb.20160401.11

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AMA Style

Xiaofang Zhao, Fuli Yao, Chunyan Zhang, Ying Cheng, Bin Xiao, et al. Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis. Cell Biol. 2016;4(1):1-8. doi: 10.11648/j.cb.20160401.11

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@article{10.11648/j.cb.20160401.11,
  author = {Xiaofang Zhao and Fuli Yao and Chunyan Zhang and Ying Cheng and Bin Xiao and Yuxiao Li and Chunyan Duan and Youping Liu and Hong Li and Rongyang Dai},
  title = {Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis},
  journal = {Cell Biology},
  volume = {4},
  number = {1},
  pages = {1-8},
  doi = {10.11648/j.cb.20160401.11},
  url = {https://doi.org/10.11648/j.cb.20160401.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20160401.11},
  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.},
 year = {2016}
}

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TY  - JOUR
T1  - Differential Activation of ER Stress Signal Pathways Contributes to Palmitate-Induced Hepatocyte Lipoapoptosis
AU  - Xiaofang Zhao
AU  - Fuli Yao
AU  - Chunyan Zhang
AU  - Ying Cheng
AU  - Bin Xiao
AU  - Yuxiao Li
AU  - Chunyan Duan
AU  - Youping Liu
AU  - Hong Li
AU  - Rongyang Dai
Y1  - 2016/04/13
PY  - 2016
N1  - https://doi.org/10.11648/j.cb.20160401.11
DO  - 10.11648/j.cb.20160401.11
T2  - Cell Biology
JF  - Cell Biology
JO  - Cell Biology
SP  - 1
EP  - 8
PB  - Science Publishing Group
SN  - 2330-0183
UR  - https://doi.org/10.11648/j.cb.20160401.11
AB  - 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.
VL  - 4
IS  - 1
ER  -

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