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

Atsushi Sakai1, Fumihito Saitow1, Motoyo Maruyama1,2

  • 1Department of Pharmacology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan.

Nature Communications
|July 6, 2017
PubMed

Insights

The miR-17-92 microRNA cluster and its members are upregulated after nerve injury, contributing to chronic neuropathic pain. Targeting these microRNAs and their potassium channel targets offers a potential therapeutic strategy for pain relief.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Chronic neuropathic pain is a debilitating condition with limited treatment options.
  • MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and play roles in various physiological and pathological processes.

Purpose of the Study:

  • To investigate the role of the miR-17-92 microRNA cluster in the development and maintenance of chronic neuropathic pain.
  • To identify the molecular mechanisms by which miR-17-92 contributes to neuropathic pain.

Main Methods:

  • Utilized a rat model of neuropathic pain induced by nerve injury.
  • Assessed the expression levels of miR-17-92 cluster members in primary sensory neurons.
  • Manipulated the expression of specific miR-17-92 members using overexpression and blockade techniques.
  • Performed single-cell analysis to identify co-expression patterns of miRNAs and their predicted targets.
  • Investigated the impact of miR-17-92 on voltage-gated potassium channels and potassium currents.
  • Evaluated the efficacy of potassium channel modulators in alleviating neuropathic pain.

Main Results:

  • All miR-17-92 cluster members were persistently upregulated in primary sensory neurons following nerve injury.
  • Overexpression of specific miR-17-92 members (miR-18a, miR-19a, miR-19b, miR-92a) induced mechanical allodynia.
  • Blockade of these miRNAs alleviated mechanical allodynia in the neuropathic pain model.
  • The miR-17-92 cluster targets genes encoding voltage-gated potassium channels and their subunits.
  • miR-17-92 downregulates potassium channel expression, leading to reduced outward potassium currents, particularly A-type currents.
  • Combined application of potassium channel modulators synergistically reduced mechanical allodynia.

Conclusions:

  • The miR-17-92 microRNA cluster plays a significant role in modulating chronic neuropathic pain.
  • miR-17-92 contributes to neuropathic pain by downregulating voltage-gated potassium channels and altering neuronal excitability.
  • Targeting the miR-17-92 cluster and its downstream potassium channel targets presents a promising therapeutic strategy for managing neuropathic pain.

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