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Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells
Apoptosis has been postulated to play an important role during feline infectious peritonitis virus (FIPV) infection; however, its mechanism is not well characterized. This study is focused on apoptosis and transcriptional profiling of FIPV-infected cells following in vitro infection of CRFK cells wi...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7088095/ https://www.ncbi.nlm.nih.gov/pubmed/26386572 http://dx.doi.org/10.1007/s10495-015-1172-7 |
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author | Shuid, Ahmad Naqib Safi, Nikoo Haghani, Amin Mehrbod, Parvaneh Haron, Mohd Syamsul Reza Tan, Sheau Wei Omar, Abdul Rahman |
author_facet | Shuid, Ahmad Naqib Safi, Nikoo Haghani, Amin Mehrbod, Parvaneh Haron, Mohd Syamsul Reza Tan, Sheau Wei Omar, Abdul Rahman |
author_sort | Shuid, Ahmad Naqib |
collection | PubMed |
description | Apoptosis has been postulated to play an important role during feline infectious peritonitis virus (FIPV) infection; however, its mechanism is not well characterized. This study is focused on apoptosis and transcriptional profiling of FIPV-infected cells following in vitro infection of CRFK cells with FIPV 79-1146 WSU. Flow cytometry was used to determine mode of cell death in first 42 h post infection (hpi). FIPV infected cells underwent early apoptosis at 9 hpi (p < 0.05) followed by late apoptosis at 12 hpi (p < 0.05) and necrosis from 24 hpi (p < 0.05). Then, next generation sequencing was performed on 9 hpi and control uninfected cells by Illumina analyzer. An aggregate of 4546 genes (2229 down-regulated and 2317 up-regulated) from 17 cellular process, 11 molecular functions and 130 possible biological pathways were affected by FIPV. 131 genes from apoptosis cluster (80 down-regulated and 51 up-regulated) along with increase of apoptosis, p53, p38 MAPK, VEGF and chemokines/cytokines signaling pathways were probably involved in apoptosis process. Six of the de-regulated genes expression (RASSF1, BATF2, MAGEB16, PDCD5, TNFα and TRAF2) and TNFα protein concentration were analyzed by RT-qPCR and ELISA, respectively, at different time-points. Up-regulations of both pro-apoptotic (i.e. PDCD5) and anti-apoptotic (i.e. TRAF2) were detected from first hpi and continuing to deregulate during apoptosis process in the infected cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10495-015-1172-7) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-7088095 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-70880952020-03-23 Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells Shuid, Ahmad Naqib Safi, Nikoo Haghani, Amin Mehrbod, Parvaneh Haron, Mohd Syamsul Reza Tan, Sheau Wei Omar, Abdul Rahman Apoptosis Original Paper Apoptosis has been postulated to play an important role during feline infectious peritonitis virus (FIPV) infection; however, its mechanism is not well characterized. This study is focused on apoptosis and transcriptional profiling of FIPV-infected cells following in vitro infection of CRFK cells with FIPV 79-1146 WSU. Flow cytometry was used to determine mode of cell death in first 42 h post infection (hpi). FIPV infected cells underwent early apoptosis at 9 hpi (p < 0.05) followed by late apoptosis at 12 hpi (p < 0.05) and necrosis from 24 hpi (p < 0.05). Then, next generation sequencing was performed on 9 hpi and control uninfected cells by Illumina analyzer. An aggregate of 4546 genes (2229 down-regulated and 2317 up-regulated) from 17 cellular process, 11 molecular functions and 130 possible biological pathways were affected by FIPV. 131 genes from apoptosis cluster (80 down-regulated and 51 up-regulated) along with increase of apoptosis, p53, p38 MAPK, VEGF and chemokines/cytokines signaling pathways were probably involved in apoptosis process. Six of the de-regulated genes expression (RASSF1, BATF2, MAGEB16, PDCD5, TNFα and TRAF2) and TNFα protein concentration were analyzed by RT-qPCR and ELISA, respectively, at different time-points. Up-regulations of both pro-apoptotic (i.e. PDCD5) and anti-apoptotic (i.e. TRAF2) were detected from first hpi and continuing to deregulate during apoptosis process in the infected cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10495-015-1172-7) contains supplementary material, which is available to authorized users. Springer US 2015-09-19 2015 /pmc/articles/PMC7088095/ /pubmed/26386572 http://dx.doi.org/10.1007/s10495-015-1172-7 Text en © Springer Science+Business Media New York 2015 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Original Paper Shuid, Ahmad Naqib Safi, Nikoo Haghani, Amin Mehrbod, Parvaneh Haron, Mohd Syamsul Reza Tan, Sheau Wei Omar, Abdul Rahman Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells |
title | Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells |
title_full | Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells |
title_fullStr | Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells |
title_full_unstemmed | Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells |
title_short | Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells |
title_sort | apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7088095/ https://www.ncbi.nlm.nih.gov/pubmed/26386572 http://dx.doi.org/10.1007/s10495-015-1172-7 |
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