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Int. J. Mol. Sci. 2015, 16(8), 19780-19795; doi:10.3390/ijms160819780

Endoplasmic Reticulum Stress Cooperates in Zearalenone-Induced Cell Death of RAW 264.7 Macrophages

1
Key Laboratory of Animal Biotechnology of the Ministry of Agriculture, Northwest Agriculture and Forestry University, Yangling 712100, Shaanxi, China
2
College of Veterinary Medicine, Northwest Agriculture and Forestry University, Yangling 712100, Shaanxi, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Masato Matsuoka
Received: 8 May 2015 / Revised: 13 July 2015 / Accepted: 14 July 2015 / Published: 20 August 2015
(This article belongs to the Special Issue Modulators of Endoplasmic Reticulum Stress)
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Abstract

Zearalenone (ZEA) is a fungal mycotoxin that causes cell apoptosis and necrosis. However, little is known about the molecular mechanisms of ZEA toxicity. The objective of this study was to explore the effects of ZEA on the proliferation and apoptosis of RAW 264.7 macrophages and to uncover the signaling pathway underlying the cytotoxicity of ZEA in RAW 264.7 macrophages. This study demonstrates that the endoplasmic reticulum (ER) stress pathway cooperated in ZEA-induced cell death of the RAW 264.7 macrophages. Our results show that ZEA treatment reduced the viability of RAW 264.7 macrophages in a dose- and time-dependent manner as shown by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay (MTT) and flow cytometry assay. Western blots analysis revealed that ZEA increased the expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP), two ER stress-related marker genes. Furthermore, treating the cells with the ER stress inhibitors 4-phenylbutyrate (4-PBA) or knocking down CHOP, using lentivirus encoded short hairpin interfering RNAs (shRNAs), significantly diminished the ZEA-induced increases in GRP78 and CHOP, and cell death. In summary, our results suggest that ZEA induces the apoptosis and necrosis of RAW 264.7 macrophages in a dose- and time-dependent manner via the ER stress pathway in which the activation of CHOP plays a critical role. View Full-Text
Keywords: zearalenone; endoplasmic reticulum stress; CHOP; RAW 264.7 macrophages zearalenone; endoplasmic reticulum stress; CHOP; RAW 264.7 macrophages
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Chen, F.; Li, Q.; Zhang, Z.; Lin, P.; Lei, L.; Wang, A.; Jin, Y. Endoplasmic Reticulum Stress Cooperates in Zearalenone-Induced Cell Death of RAW 264.7 Macrophages. Int. J. Mol. Sci. 2015, 16, 19780-19795.

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