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

Atsushi Sakai (), Fumihito Saitow, Motoyo Maruyama, Noriko Miyake, Koichi Miyake, Takashi Shimada, Takashi Okada and Hidenori Suzuki
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Atsushi Sakai: Nippon Medical School
Fumihito Saitow: Nippon Medical School
Motoyo Maruyama: 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

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms16079

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