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miR-342-5p targets CTNNBIP1 to promote enterovirus 71 replication

Chengyan Tang1, Yu Chen2, Hongjiao Jin2

  • 1Suzhou Medical College of Soochow University, Suzhou, 215123, People's Republic of China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, People's Republic of China; Department of Pediatric Surgery, Guizhou Children's Hospital, Zunyi, 563000, People's Republic of China.

Microbial Pathogenesis
|July 21, 2023
PubMed
Abstract

Insights

MicroRNA miR-342-5p promotes enterovirus 71 (EV71) replication and impairs the innate immune response. This occurs by targeting CTNNBIP1, influencing the Wnt/CTNNB1 signaling pathway and type I interferon production.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Enterovirus 71 (EV71) is a significant human pathogen causing severe neurological diseases.
  • The role of microRNAs (miRNAs) in viral replication and host immune response is increasingly recognized.
  • miR-342-5p has been implicated in various cellular processes, but its specific function in EV71 infection requires elucidation.

Purpose of the Study:

  • To investigate the role of miR-342-5p in the replication of Enterovirus 71 (EV71).
  • To elucidate the underlying molecular mechanisms by which miR-342-5p influences EV71 infection and the host immune response.

Main Methods:

  • EV71 infection in suckling mice and HMC3 cells.
  • Transcriptome sequencing for differential gene and miRNA analysis.
  • Dual luciferase reporter assay to confirm target gene binding.
  • Cell viability assays (CCK-8).
  • Molecular assays including RT-qPCR, Western blot, immunofluorescence, and immunohistochemistry to assess viral protein levels and inflammatory markers.

Main Results:

  • Transcriptome analysis revealed the involvement of the Wnt pathway and identified CTNNBIP1 as a target of miR-342-5p.
  • Overexpression of miR-342-5p significantly promoted EV71 VP1 mRNA and protein expression in cells and mouse spinal cord tissues.
  • miR-342-5p overexpression elevated pro-inflammatory cytokines (TNF-α, IL-6, IL-10) and suppressed antiviral interferon-beta (IFN-β) levels.
  • Highly expressed miR-342-5p disrupted neuronal structure and reduced glial cell numbers.
  • Overexpressed CTNNBIP1 counteracted the effects of miR-342-5p, reducing viral replication and modulating cytokine profiles.
  • The mechanism involves miR-342-5p targeting CTNNBIP1, inhibiting its expression, and subsequently enhancing the Wnt/CTNNB1/TCF4 interaction, leading to altered type I interferon response.

Conclusions:

  • miR-342-5p acts as a positive regulator of EV71 replication in nerve cells and tissues.
  • Overexpression of miR-342-5p attenuates the innate antiviral immune response through the Wnt/CTNNB1 signaling pathway.
  • Targeting miR-342-5p or modulating the Wnt pathway may offer therapeutic strategies against EV71 infections.
Keywords:
Enterovirus 71Foot and mouth diseaseHandViral replicationWnt signaling pathwaymiR-342-5p

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