TITLE:
miR-362-3p Knockdown Triggers Inflammation to Promote Neuropathic Pain by Modulating JMJD1A Expression
AUTHORS:
Miao Huo, Qian Zhang, Xingxing Zheng, Hui Wang, Guang Yang, Jiao Guo, Ziyu Zhao
KEYWORDS:
miR-362-3p, Neuropathic Pain, Neuroinflammation, JMJD1A, Rats
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.13 No.8,
August
30,
2022
ABSTRACT: Objective: When nerve
injury or inflammatory injury, different miRNA-mediated signal pathways are activated or inactivated,
causing pain or hyperalgesia. Therefore, miRNA has become a new direction of pain
mechanism research. We aimed to investigate the effect and mechanism of
miR-362-3p on neuropathic pain in rats with chronic sciatic nerve injury (CCI). Methods: Neuropathic pain CCI rat model was established. Real-time-quantitative
polymerase chain reaction (RT-PCR), Western
blot, immunofluorescence, intrathecal injection, Enzyme-linked
immunosorbent assay (ELISA), and dual luciferase reporter gene assays were used
to explore the role of miR-362-3p in neuropathic pain development and the
relationship between miR-362-3p and JMJD1A (Jumonji domain-containing 1A). Results: In the CCI group, the miR-362-3p level was increased and JMJD1A level was
reduced in spinal cords and isolated microglia. The paw withdrawal threshold
(PWT) and paw withdrawal latency (PWL) values were increased, the secretion of
inflammatory factors was reduced, and the microglial marker Iba1 expression was
decreased after intrathecal administration of miR-362-3p. miR-362-3p was
observed to target JMJD1A. JMJD1A elevation abolished the inhibitory effects of
miR-362-3p on neuropathic pain development. Conclusion: Intrathecal administration of miR-362-3p significantly relieved
neuropathic pain in CCI rats and inhibited neuroinflammation possibly
through regulating JMJD1A.