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MicroRNA cluster miR-17-92 regulates multiple functionally related voltage-gated potassium channels in chronic neuropathic pain

Author

Listed:
  • Atsushi Sakai

    (Nippon Medical School)

  • Fumihito Saitow

    (Nippon Medical School)

  • Motoyo Maruyama

    (Nippon Medical School
    Nippon Medical School)

  • Noriko Miyake

    (Nippon Medical School)

  • Koichi Miyake

    (Nippon Medical School)

  • Takashi Shimada

    (Nippon Medical School)

  • Takashi Okada

    (Nippon Medical School)

  • Hidenori Suzuki

    (Nippon Medical School)

Abstract

miR-17-92 is a microRNA cluster with six distinct members. Here, we show that the miR-17-92 cluster and its individual members modulate chronic neuropathic pain. All cluster members are persistently upregulated in primary sensory neurons after nerve injury. Overexpression of miR-18a, miR-19a, miR-19b and miR-92a cluster members elicits mechanical allodynia in rats, while their blockade alleviates mechanical allodynia in a rat model of neuropathic pain. Plausible targets for the miR-17-92 cluster include genes encoding numerous voltage-gated potassium channels and their modulatory subunits. Single-cell analysis reveals extensive co-expression of miR-17-92 cluster and its predicted targets in primary sensory neurons. miR-17-92 downregulates the expression of potassium channels, and reduced outward potassium currents, in particular A-type currents. Combined application of potassium channel modulators synergistically alleviates mechanical allodynia induced by nerve injury or miR-17-92 overexpression. miR-17-92 cluster appears to cooperatively regulate the function of multiple voltage-gated potassium channel subunits, perpetuating mechanical allodynia.

Suggested Citation

  • Atsushi Sakai & Fumihito Saitow & Motoyo Maruyama & Noriko Miyake & Koichi Miyake & Takashi Shimada & Takashi Okada & Hidenori Suzuki, 2017. "MicroRNA cluster miR-17-92 regulates multiple functionally related voltage-gated potassium channels in chronic neuropathic pain," Nature Communications, Nature, vol. 8(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms16079
    DOI: 10.1038/ncomms16079
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