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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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2022-09-01
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Series: | Frontiers in Microbiology |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fmicb.2022.988259/full |
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author | Yujuan Niu Zhiyang Liu Mengyu Wang Ke Du Kaihui Chang Yonghe Ding |
author_facet | Yujuan Niu Zhiyang Liu Mengyu Wang Ke Du Kaihui Chang Yonghe Ding |
author_sort | Yujuan Niu |
collection | DOAJ |
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. |
first_indexed | 2024-04-12T21:10:18Z |
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id | doaj.art-3d2d80a3f8ef4444b385b0f49d5bde45 |
institution | Directory Open Access Journal |
issn | 1664-302X |
language | English |
last_indexed | 2024-04-12T21:10:18Z |
publishDate | 2022-09-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Microbiology |
spelling | doaj.art-3d2d80a3f8ef4444b385b0f49d5bde452022-12-22T03:16:36ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2022-09-011310.3389/fmicb.2022.988259988259TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cellYujuan NiuZhiyang LiuMengyu WangKe DuKaihui ChangYonghe DingFowl 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.https://www.frontiersin.org/articles/10.3389/fmicb.2022.988259/fullproteomicsFAdV-4LMH cellsTMTNotch signalinginflammatory and immune response |
spellingShingle | Yujuan Niu Zhiyang Liu Mengyu Wang Ke Du Kaihui Chang Yonghe Ding TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell Frontiers in Microbiology proteomics FAdV-4 LMH cells TMT Notch signaling inflammatory and immune response |
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 | proteomics FAdV-4 LMH cells TMT Notch signaling inflammatory and immune response |
url | https://www.frontiersin.org/articles/10.3389/fmicb.2022.988259/full |
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