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Dengue 2 infection of HepG2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death
BACKGROUND: A number of studies have implicated the direct involvement of the liver in dengue virus (DENV) infection, and it has been widely shown that liver cells subsequently undergo apoptosis. The mechanism by which liver cells undergo apoptosis in response to DENV infection remains unclear. To p...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847886/ https://www.ncbi.nlm.nih.gov/pubmed/24034452 http://dx.doi.org/10.1186/1756-0500-6-372 |
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author | Thepparit, Chutima Khakpoor, Atefeh Khongwichit, Sarawut Wikan, Nitwara Fongsaran, Chanida Chingsuwanrote, Pimjai Panraksa, Patcharee Smith, Duncan R |
author_facet | Thepparit, Chutima Khakpoor, Atefeh Khongwichit, Sarawut Wikan, Nitwara Fongsaran, Chanida Chingsuwanrote, Pimjai Panraksa, Patcharee Smith, Duncan R |
author_sort | Thepparit, Chutima |
collection | PubMed |
description | BACKGROUND: A number of studies have implicated the direct involvement of the liver in dengue virus (DENV) infection, and it has been widely shown that liver cells subsequently undergo apoptosis. The mechanism by which liver cells undergo apoptosis in response to DENV infection remains unclear. To provide further information on the mechanism of apoptosis in DENV infected liver cells, HepG2 cells were infected with DENV 2 and analyzed for the induction of ER stress, apoptosis and autophagy. RESULTS: In response to DENV infection, HepG2 cells showed the induction of both the ER resident unfolded protein response as well as the Noxa/PUMA stress response pathways. Proteolytic activation of caspases 4, 7, 8 and 9 was observed as well as changes in mitochondrial transmembrane potential. Increased monodansylcadaverine staining was observed in DENV infected cells, consistent with the previously reported induction of autophagy. CONCLUSIONS: These results are consistent with a model in which the induction of multiple ER stress pathways is coupled with the induction of multiple cell death pathways as a mechanism to ensure the removal of infected liver cells from the system. |
format | Online Article Text |
id | pubmed-3847886 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-38478862013-12-04 Dengue 2 infection of HepG2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death Thepparit, Chutima Khakpoor, Atefeh Khongwichit, Sarawut Wikan, Nitwara Fongsaran, Chanida Chingsuwanrote, Pimjai Panraksa, Patcharee Smith, Duncan R BMC Res Notes Research Article BACKGROUND: A number of studies have implicated the direct involvement of the liver in dengue virus (DENV) infection, and it has been widely shown that liver cells subsequently undergo apoptosis. The mechanism by which liver cells undergo apoptosis in response to DENV infection remains unclear. To provide further information on the mechanism of apoptosis in DENV infected liver cells, HepG2 cells were infected with DENV 2 and analyzed for the induction of ER stress, apoptosis and autophagy. RESULTS: In response to DENV infection, HepG2 cells showed the induction of both the ER resident unfolded protein response as well as the Noxa/PUMA stress response pathways. Proteolytic activation of caspases 4, 7, 8 and 9 was observed as well as changes in mitochondrial transmembrane potential. Increased monodansylcadaverine staining was observed in DENV infected cells, consistent with the previously reported induction of autophagy. CONCLUSIONS: These results are consistent with a model in which the induction of multiple ER stress pathways is coupled with the induction of multiple cell death pathways as a mechanism to ensure the removal of infected liver cells from the system. BioMed Central 2013-09-14 /pmc/articles/PMC3847886/ /pubmed/24034452 http://dx.doi.org/10.1186/1756-0500-6-372 Text en Copyright © 2013 Thepparit et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Thepparit, Chutima Khakpoor, Atefeh Khongwichit, Sarawut Wikan, Nitwara Fongsaran, Chanida Chingsuwanrote, Pimjai Panraksa, Patcharee Smith, Duncan R Dengue 2 infection of HepG2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death |
title | Dengue 2 infection of HepG2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death |
title_full | Dengue 2 infection of HepG2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death |
title_fullStr | Dengue 2 infection of HepG2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death |
title_full_unstemmed | Dengue 2 infection of HepG2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death |
title_short | Dengue 2 infection of HepG2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death |
title_sort | dengue 2 infection of hepg2 liver cells results in endoplasmic reticulum stress and induction of multiple pathways of cell death |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847886/ https://www.ncbi.nlm.nih.gov/pubmed/24034452 http://dx.doi.org/10.1186/1756-0500-6-372 |
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