Beta-catenin inhibits bovine parainfluenza virus type 3 replication via innate immunity pathway.

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  • Author(s): Du X;Du X; He W; He W; He H; He H; Wang H; Wang H
  • Source:
    BMC veterinary research [BMC Vet Res] 2020 Mar 03; Vol. 16 (1), pp. 72. Date of Electronic Publication: 2020 Mar 03.
  • Publication Type:
    Journal Article
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: BioMed Central Country of Publication: England NLM ID: 101249759 Publication Model: Electronic Cited Medium: Internet ISSN: 1746-6148 (Electronic) Linking ISSN: 17466148 NLM ISO Abbreviation: BMC Vet Res Subsets: MEDLINE
    • Publication Information:
      Original Publication: London : BioMed Central, 2005-
    • Subject Terms:
      Immunity, Innate*; Parainfluenza Virus 3, Bovine/*drug effects ; Virus Replication/*drug effects ; beta Catenin/*metabolism; Animals ; Cattle ; Cell Line ; Glycogen Synthase Kinase 3 beta/drug effects ; Lithium Chloride/pharmacology ; RNA, Messenger ; Respirovirus Infections/immunology ; Respirovirus Infections/veterinary ; Signal Transduction ; beta Catenin/genetics
    • Abstract:
      Background: Bovine parainfluenza virus type 3 (BPIV3) is one of the important viral respiratory agents associated with the bovine respiratory disease complex (BRDC) in cattle. Previous study has demonstrated that infection of BPIV3 causes innate immune response within the host cell. β-catenin is a key component of the Wnt/β-catenin signal pathway which is involved in the regulation of interferon-beta (IFN-β) transcription. Some viruses can activate while others can inhibit the Wnt/β-catenin signaling pathway. However, the role of β-catenin in BPIV3 infection remains unclear.
      Results: Here we found that the expression of β-catenin mRNA was up-regulated and β-catenin protein was down-regulated after BPIV3 infection in MDBK cells. Moreover, it was confirmed that overexpression of β-catenin suppressed BPIV3 replication and knockdown of β-catenin promoted viral replication, suggesting that β-catenin inhibits BPIV3 replication. Furthermore, IFN-β signal pathway and virus titer analysis using the GSK3β inhibitor (LiCl) revealed that Wnt/β-catenin can serve as a mechanism to suppress virus replication in infected cells. The results indicated that LiCl promoted the expression and accumulation in the nucleus of β-catenin, which further promoted the expression of IFN-β and OSA1 and suppressed BPIV3 replication. Most importantly, BPIV3 down-regulating β-catenin protein expression was due to degradation of GSK3β mediated proteasome pathway.
      Conclusions: In summary, we discovered the relationship between β-catenin and BPIV3 replication. These results provided further insight into the study of BPIV3 pathogenesis.
    • References:
      Annu Rev Pathol. 2018 Jan 24;13:351-378. (PMID: 29125798)
      PLoS One. 2013 Oct 10;8(10):e77865. (PMID: 24130899)
      Elife. 2019 Feb 05;8:. (PMID: 30717826)
      Virology. 2015 Feb;476:134-140. (PMID: 25543964)
      Nat Rev Immunol. 2012 Jan 06;12(2):125-35. (PMID: 22222875)
      Development. 2019 Jul 2;146(13):. (PMID: 31189665)
      Vet Microbiol. 2015 Jul 9;178(1-2):61-9. (PMID: 25960335)
      J Hepatol. 2009 Nov;51(5):853-64. (PMID: 19726098)
      J Cell Biochem. 2019 Aug;120(8):12519-12533. (PMID: 31016779)
      Vet Microbiol. 2019 Dec;239:108456. (PMID: 31767082)
      BMC Vet Res. 2018 Jan 04;14(1):3. (PMID: 29301517)
      Cell Mol Immunol. 2016 Jan;13(1):11-35. (PMID: 25544499)
      Virology. 2017 Jan;500:91-95. (PMID: 27788397)
      Vet Microbiol. 2020 Jan;240:108510. (PMID: 31902512)
      Cell Mol Immunol. 2019 Oct;16(10):800-809. (PMID: 29973649)
      Cell Prolif. 2018 Oct;51(5):e12464. (PMID: 30004146)
      Oncotarget. 2017 May 16;8(20):33972-33989. (PMID: 28430641)
      PLoS One. 2018 Jan 11;13(1):e0191010. (PMID: 29324866)
      PLoS Pathog. 2012;8(10):e1002959. (PMID: 23071438)
      J Cell Mol Med. 2018 Jan;22(1):589-599. (PMID: 29024409)
      Arch Virol. 2017 Oct;162(10):2937-2947. (PMID: 28685286)
      Pathogens. 2019 Feb 25;8(1):. (PMID: 30823555)
      J Virol. 2008 Mar;82(6):2813-20. (PMID: 18199649)
      Biotechnol Prog. 2015 Mar-Apr;31(2):452-9. (PMID: 25395261)
      Cancer Biomark. 2019;25(1):115-126. (PMID: 31006667)
      J Virol. 2012 Feb;86(4):1911-21. (PMID: 22156527)
      Mol Cell Biol. 2015 Oct 12;36(1):13-29. (PMID: 26459757)
      Vet Microbiol. 2019 Jun;233:174-183. (PMID: 31176405)
      Vet Microbiol. 2019 Dec;239:108494. (PMID: 31767068)
      Front Microbiol. 2018 Mar 12;9:390. (PMID: 29593670)
      Immunity. 2014 Jan 16;40(1):13-24. (PMID: 24439265)
      Oncol Lett. 2016 Dec;12(6):4623-4629. (PMID: 28105169)
      Mediators Inflamm. 2010;2010:184328. (PMID: 20672047)
      Pharmacol Ther. 2019 Apr;196:79-90. (PMID: 30468742)
      Gastroenterology. 2019 Jan;156(2):369-383. (PMID: 30267712)
      Annu Rev Immunol. 2014;32:513-45. (PMID: 24555472)
      J Virol. 2019 May 15;93(11):. (PMID: 30867312)
      Mol Cancer. 2008 Feb 18;7:21. (PMID: 18282277)
    • Grant Information:
      31872490 National Natural Science Fund of China
    • Contributed Indexing:
      Keywords: Bovine parainfluenza virus type 3 (BPIV3); GSK3β; Viral replication; Wnt/β-catenin signal pathway; β-Catenin
    • Accession Number:
      0 (RNA, Messenger)
      0 (beta Catenin)
      EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
      G4962QA067 (Lithium Chloride)
    • Publication Date:
      Date Created: 20200305 Date Completed: 20201029 Latest Revision: 20201029
    • Publication Date:
      20240829
    • Accession Number:
      PMC7055115
    • Accession Number:
      10.1186/s12917-020-02291-w
    • Accession Number:
      32127006