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MiR-9 promotes microglial activation by targeting MCPIP1

Author

Listed:
  • Honghong Yao

    (Medical School of Southeast University)

  • Rong Ma

    (University of Nebraska Medical Center)

  • Lu Yang

    (University of Nebraska Medical Center)

  • Guoku Hu

    (University of Nebraska Medical Center)

  • Xufeng Chen

    (The first Affiliated Hospital of Nanjing Medical University)

  • Ming Duan

    (Key Laboratory for Zoonosis Research, Ministry of Education, Jilin University)

  • Yeonhee Kook

    (University of Nebraska Medical Center)

  • Fang Niu

    (University of Nebraska Medical Center)

  • Ke Liao

    (University of Nebraska Medical Center)

  • Minggui Fu

    (School of Medicine, University of Missouri-Kansas City)

  • Gang Hu

    (Jiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University)

  • Pappachan Kolattukudy

    (Burnett School of Biomedical Science, College of Medicine, University of Central Florida)

  • Shilpa Buch

    (University of Nebraska Medical Center)

Abstract

Microglia participate in innate inflammatory responses within the central nervous system. The highly conserved microRNA-9 (miR-9) plays critical roles in neurogenesis as well as axonal extension. Its role in microglial inflammatory responses, however, remains poorly understood. Here we identify a unique role of miR-9 in mediating the microglial inflammatory response via distinct signalling pathways. MiR-9-mediated regulation of cellular activation involved downregulated expression of the target protein, monocyte chemotactic protein-induced protein 1 (MCPIP1) that is crucial for controlling inflammation. Results indicate that miR-9-mediated cellular activation involved signalling via the NF-κB pathway, but not the β-catenin pathway.

Suggested Citation

  • Honghong Yao & Rong Ma & Lu Yang & Guoku Hu & Xufeng Chen & Ming Duan & Yeonhee Kook & Fang Niu & Ke Liao & Minggui Fu & Gang Hu & Pappachan Kolattukudy & Shilpa Buch, 2014. "MiR-9 promotes microglial activation by targeting MCPIP1," Nature Communications, Nature, vol. 5(1), pages 1-12, September.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5386
    DOI: 10.1038/ncomms5386
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