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Mitophagy in TGEV infection counteracts oxidative stress and apoptosis
The intestinal epithelial cells contain a large number of mitochondria for persisting absorption and barrier function. Selective autophagy of mitochondria (mitophagy) plays an important role in the quality control of mitochondria and maintenance of cell homeostasis. Transmissible gastroenteritis vir...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053637/ https://www.ncbi.nlm.nih.gov/pubmed/27027356 http://dx.doi.org/10.18632/oncotarget.8345 |
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author | Zhu, Liqi Mou, Chunxiao Yang, Xing Lin, Jian Yang, Qian |
author_facet | Zhu, Liqi Mou, Chunxiao Yang, Xing Lin, Jian Yang, Qian |
author_sort | Zhu, Liqi |
collection | PubMed |
description | The intestinal epithelial cells contain a large number of mitochondria for persisting absorption and barrier function. Selective autophagy of mitochondria (mitophagy) plays an important role in the quality control of mitochondria and maintenance of cell homeostasis. Transmissible gastroenteritis virus (TGEV) is a porcine enteropathogenic coronavirus which induces malabsorption and lethal watery diarrhea in suckling piglets. The role of mitophagy in the pathological changes caused by TGEV infection is unclear. Here, we report that TGEV induces mitophagy to suppress oxidative stress and apoptosis induced by viral infection in porcine epithelial cells (IPEC-J2). We observe that TGEV infection induce mitochondrial injury, abnormal morphology, complete mitophagy, and without obvious apoptosis after TGEV infection. Meanwhile, TGEV also induces DJ-1 and some antioxidant genes upregulation to suppress oxidative stress induced by viral infection. Furthermore, silencing DJ-1 inhibit mitophagy and increase apoptosis after TGEV infection. In addition, we demonstrate for the first time that viral nucleocapsid protein (N) is located in mitochondria and mitophagosome during virus infection or be expressed alone. Those results provide a novel perspective for further improvement of prevention and treatment in TGEV infection. These results suggest that TGEV infection induce mitophagy to promote cell survival and possibly viral infection. |
format | Online Article Text |
id | pubmed-5053637 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-50536372016-10-12 Mitophagy in TGEV infection counteracts oxidative stress and apoptosis Zhu, Liqi Mou, Chunxiao Yang, Xing Lin, Jian Yang, Qian Oncotarget Research Paper The intestinal epithelial cells contain a large number of mitochondria for persisting absorption and barrier function. Selective autophagy of mitochondria (mitophagy) plays an important role in the quality control of mitochondria and maintenance of cell homeostasis. Transmissible gastroenteritis virus (TGEV) is a porcine enteropathogenic coronavirus which induces malabsorption and lethal watery diarrhea in suckling piglets. The role of mitophagy in the pathological changes caused by TGEV infection is unclear. Here, we report that TGEV induces mitophagy to suppress oxidative stress and apoptosis induced by viral infection in porcine epithelial cells (IPEC-J2). We observe that TGEV infection induce mitochondrial injury, abnormal morphology, complete mitophagy, and without obvious apoptosis after TGEV infection. Meanwhile, TGEV also induces DJ-1 and some antioxidant genes upregulation to suppress oxidative stress induced by viral infection. Furthermore, silencing DJ-1 inhibit mitophagy and increase apoptosis after TGEV infection. In addition, we demonstrate for the first time that viral nucleocapsid protein (N) is located in mitochondria and mitophagosome during virus infection or be expressed alone. Those results provide a novel perspective for further improvement of prevention and treatment in TGEV infection. These results suggest that TGEV infection induce mitophagy to promote cell survival and possibly viral infection. Impact Journals LLC 2016-03-24 /pmc/articles/PMC5053637/ /pubmed/27027356 http://dx.doi.org/10.18632/oncotarget.8345 Text en Copyright: © 2016 Zhu et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Zhu, Liqi Mou, Chunxiao Yang, Xing Lin, Jian Yang, Qian Mitophagy in TGEV infection counteracts oxidative stress and apoptosis |
title | Mitophagy in TGEV infection counteracts oxidative stress and apoptosis |
title_full | Mitophagy in TGEV infection counteracts oxidative stress and apoptosis |
title_fullStr | Mitophagy in TGEV infection counteracts oxidative stress and apoptosis |
title_full_unstemmed | Mitophagy in TGEV infection counteracts oxidative stress and apoptosis |
title_short | Mitophagy in TGEV infection counteracts oxidative stress and apoptosis |
title_sort | mitophagy in tgev infection counteracts oxidative stress and apoptosis |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053637/ https://www.ncbi.nlm.nih.gov/pubmed/27027356 http://dx.doi.org/10.18632/oncotarget.8345 |
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