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TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell

Fowl adenovirus serotype 4 (FAdV-4) is recognized as a pathogen that causes hydropericardium syndrome. Irrespective of the pathway used by the virus to invade the chicken, the pathological characteristics of the disease include degeneration and necrosis of hepatocytes, formation of intranuclear incl...

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Autores principales: Niu, Yujuan, Liu, Zhiyang, Wang, Mengyu, Du, Ke, Chang, Kaihui, Ding, Yonghe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9520525/
https://www.ncbi.nlm.nih.gov/pubmed/36187945
http://dx.doi.org/10.3389/fmicb.2022.988259
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author Niu, Yujuan
Liu, Zhiyang
Wang, Mengyu
Du, Ke
Chang, Kaihui
Ding, Yonghe
author_facet Niu, Yujuan
Liu, Zhiyang
Wang, Mengyu
Du, Ke
Chang, Kaihui
Ding, Yonghe
author_sort Niu, Yujuan
collection PubMed
description Fowl adenovirus serotype 4 (FAdV-4) is recognized as a pathogen that causes hydropericardium syndrome. Irrespective of the pathway used by the virus to invade the chicken, the pathological characteristics of the disease include degeneration and necrosis of hepatocytes, formation of intranuclear inclusions, as well as inflammatory cell infiltration. Liver dysfunction constitutes one of the critical factors leading to death. Therefore, it is vital to investigate the virus-mediated severe pathological liver damage to further understand the pathogenesis of FAdV-4. Here, proteomics, a tandem mass tag (TMT)-based approach to directly analyze protein expression, was used to determine the protein expression during FAdV-4 proliferation in leghorn male hepatoma (LMH) cells. We identified 177 differentially expressed proteins associated with various biological processes and pathways. The functional enrichment analysis revealed that FAdV-4 could downregulate some signaling pathways in LMH cells, including NOD-like receptor signaling, RIG-I-like receptor signaling, NF-κB signaling, TNF signaling pathway, and Notch signaling, FoxO signaling, PI3K-Akt signaling, and autophagy. The results of proteomics screening suggested an association between FAdV-4 infection and Notch signaling in LMH in vitro, indicating that Notch signaling regulated the expression of inflammatory cytokines and interferons but not viral replication in LMH cells. These data contributed to the understanding of the immunopathogenesis and inflammopathogenesis of FAdV-4 infection and also provided valuable information for the further analysis of the molecular mechanisms underlying viral pathogenesis.
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spelling pubmed-95205252022-09-30 TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell Niu, Yujuan Liu, Zhiyang Wang, Mengyu Du, Ke Chang, Kaihui Ding, Yonghe Front Microbiol Microbiology Fowl adenovirus serotype 4 (FAdV-4) is recognized as a pathogen that causes hydropericardium syndrome. Irrespective of the pathway used by the virus to invade the chicken, the pathological characteristics of the disease include degeneration and necrosis of hepatocytes, formation of intranuclear inclusions, as well as inflammatory cell infiltration. Liver dysfunction constitutes one of the critical factors leading to death. Therefore, it is vital to investigate the virus-mediated severe pathological liver damage to further understand the pathogenesis of FAdV-4. Here, proteomics, a tandem mass tag (TMT)-based approach to directly analyze protein expression, was used to determine the protein expression during FAdV-4 proliferation in leghorn male hepatoma (LMH) cells. We identified 177 differentially expressed proteins associated with various biological processes and pathways. The functional enrichment analysis revealed that FAdV-4 could downregulate some signaling pathways in LMH cells, including NOD-like receptor signaling, RIG-I-like receptor signaling, NF-κB signaling, TNF signaling pathway, and Notch signaling, FoxO signaling, PI3K-Akt signaling, and autophagy. The results of proteomics screening suggested an association between FAdV-4 infection and Notch signaling in LMH in vitro, indicating that Notch signaling regulated the expression of inflammatory cytokines and interferons but not viral replication in LMH cells. These data contributed to the understanding of the immunopathogenesis and inflammopathogenesis of FAdV-4 infection and also provided valuable information for the further analysis of the molecular mechanisms underlying viral pathogenesis. Frontiers Media S.A. 2022-09-15 /pmc/articles/PMC9520525/ /pubmed/36187945 http://dx.doi.org/10.3389/fmicb.2022.988259 Text en Copyright © 2022 Niu, Liu, Wang, Du, Chang and Ding. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Niu, Yujuan
Liu, Zhiyang
Wang, Mengyu
Du, Ke
Chang, Kaihui
Ding, Yonghe
TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell
title TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell
title_full TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell
title_fullStr TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell
title_full_unstemmed TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell
title_short TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell
title_sort tmt-based quantitative proteomics analysis reveals the role of notch signaling in fadv-4-infected lmh cell
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9520525/
https://www.ncbi.nlm.nih.gov/pubmed/36187945
http://dx.doi.org/10.3389/fmicb.2022.988259
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