Abstract:
:Porcine circovirus type 3 (PCV3) infection induces porcine dermatitis and nephropathy syndrome, reproductive failure, and multisystemic inflammatory lesions in piglets and sows. To better understand the host responses to PCV3 infection, isobaric tags for relative and absolute quantification (iTRAQ) labeling combined with LC-MS/MS analysis was used for quantitative determination of differentially regulated cellular proteins in the lungs of specific-pathogen-free piglets after 4 weeks of PCV3 infection. Totally, 3429 proteins were detected in three independent mass spectrometry analyses, of which 242 differential cellular proteins were significantly regulated, consisting of 100 upregulated proteins and 142 downregulated proteins in PCV3-infected group relative to control group. Bioinformatics analysis revealed that these higher or lower abundant proteins involved primarily metabolic processes, innate immune response, MHC-I and MHC-II components, and phagosome pathways. Ten genes encoding differentially regulated proteins were selected for investigation via real-time RT-PCR. The expression levels of six representative proteins, OAS1, Mx1, ISG15, IFIT3, SOD2, and HSP60, were further confirmed by Western blotting and immunohistochemistry. This study attempted for the first time to investigate the protein profile of PCV3-infected piglets using iTRAQ technology; our findings provide valuable information to better understand the mechanisms underlying the host responses to PCV3 infection in piglets. SIGNIFICANCE: Our study identified differentially abundant proteins related to a variety of potential signaling pathways in the lungs of PCV3-infected piglets. These findings provide valuable information to better understand the mechanisms of host responses to PCV3 infection.
journal_name
J Proteomicsjournal_title
Journal of proteomicsauthors
Jiang H,Wei L,Wang D,Wang J,Zhu S,She R,Liu T,Tian J,Quan R,Hou L,Li Z,Chu J,Zhou J,Guo Y,Xi Y,Song H,Yuan F,Liu Jdoi
10.1016/j.jprot.2019.103598subject
Has Abstractpub_date
2020-02-10 00:00:00pages
103598eissn
1874-3919issn
1876-7737pii
S1874-3919(19)30370-7journal_volume
212pub_type
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