SIGIRR suppresses hepatitis B virus X protein-induced chronic inflammation in hepatocytes.

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  • Additional Information
    • Source:
      Publisher: Elsevier/North-Holland Country of Publication: Netherlands NLM ID: 7706761 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-0038 (Electronic) Linking ISSN: 03781119 NLM ISO Abbreviation: Gene Subsets: MEDLINE
    • Publication Information:
      Original Publication: Amsterdam, Elsevier/North-Holland, 1976-
    • Subject Terms:
      Hepatocytes*/metabolism ; Hepatocytes*/virology ; Receptors, Interleukin-1*/metabolism ; Receptors, Interleukin-1*/genetics ; Myeloid Differentiation Factor 88*/metabolism ; Myeloid Differentiation Factor 88*/genetics ; Viral Regulatory and Accessory Proteins* ; NF-kappa B*/metabolism ; Hepatitis B virus*/physiology ; Trans-Activators*/genetics ; Trans-Activators*/metabolism ; Inflammation*/metabolism ; Inflammation*/genetics ; Signal Transduction*; Humans ; Hepatitis B, Chronic/virology ; Hepatitis B, Chronic/genetics ; Hepatitis B, Chronic/metabolism ; Virus Replication ; Lipopolysaccharides ; Hep G2 Cells ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/virology
    • Abstract:
      Although antiviral drugs can effectively inhibit hepatitis B virus (HBV) replication, the maintenance of chronic inflammation in the liver is still considered to be an important cause for the progression of HBV-related liver disease to liver fibrosis and advanced liver disease. As an endogenous inhibitory receptor of IL-1R and TLR signaling pathways, single immunoglobulin interleukin-1-related receptor (SIGIRR) has been proven to reduce inflammation in tissues to maintain system homeostasis. However, the relationship between SIGIRR expression and HBV replication and inflammatory pathway activation in hepatocytes remains unclear. In this study, hepatitis B virus X protein (HBx) upregulated MyD88 in liver cells, promoting NF-κB signaling and inflammatory factor production with LPS treatment, and the cell supernatant accelerated the activation and collagen secretion of hepatic stellate cells. However, SIGIRR overexpression suppressed HBx-mediated MyD88/NF-κB inflammatory signaling activation and inflammatory cytokine production induced by LPS in hepatocytes and HBV replication hepatocytes. Although we did not find any effect of SIGIRR on HBV replication in vitro, this study investigated the role of SIGIRR in blocking the proinflammatory function of HBx, which may provide a new idea for the treatment of chronic hepatitis B.
      Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
      (Copyright © 2024 Elsevier B.V. All rights reserved.)
    • Contributed Indexing:
      Keywords: Chronic inflammation; Hepatitis B virus; Liver fibrogenesis; NF-κB signaling; Single immunoglobulin interleukin-1-related receptor
    • Accession Number:
      0 (hepatitis B virus X protein)
      0 (Receptors, Interleukin-1)
      0 (SIGIRR protein, human)
      0 (Myeloid Differentiation Factor 88)
      0 (Viral Regulatory and Accessory Proteins)
      0 (NF-kappa B)
      0 (Trans-Activators)
      0 (MYD88 protein, human)
      0 (Lipopolysaccharides)
    • Publication Date:
      Date Created: 20240716 Date Completed: 20240815 Latest Revision: 20240924
    • Publication Date:
      20240924
    • Accession Number:
      10.1016/j.gene.2024.148768
    • Accession Number:
      39013482