miR-106b-5p downregulate KCNQ2 expression contributing to incisional pain in male rats.

The Kv7 (KCNQ) K+ channels family controls neuron excitability, making them significant targets in pain management. This study aims to investigate the potential role of Kv7.2 (KCNQ2) in regulating postoperative pain and elucidates its upstream regulatory mechanism. A plantar incision model was established in adult male Sprague-Dawley rats to examine changes in KCNQ2 expression in dorsal root ganglion (DRG) neurons. The results demonstrated that the expression of KCNQ2 in peripheral DRG neurons decreased 4 h and 1 day post-incision. Co-staining of KCNQ2 with CGRP and IB4 was significantly reduced in the incision group. In electrophysiological experiments, XE991 depolarized the resting membrane potential of neurons in the contralateral DRGs, while retigabine hyperpolarized neurons in the ipsilateral incision DRGs. The increased excitability observed following the incision is due to a reduction in M-current. Retigabine significantly reduced Cumulative Pain Score (CPS) and increased Mechanical Withdrawal Threshold (MWT) and Thermal Withdrawal Latency (TWL) at 4 h and 1 day post-incision. Interfering with miR-106b-5p using an adeno-associated virus (AAV) increased the KCNQ2 expression in DRG one day after plantar incision, significantly reduced CPS, and increased MWT and TWL at 4 h and 1 day post-incision. These results suggested that the KCNQ2 ion channel, regulated by miR-106b-5p in the rat dorsal root ganglion (DRG), maybe a target for treating plantar incision pain. PERSPECTIVE: This study elucidates the role of KCNQ2 in modulating incisional pain, providing valuable insights that may aid basic researchers in further exploring pain mechanisms and developing targeted therapeutic strategies.