Knockdown of Linc00052 alleviated spinal nerve ligation‐triggered neuropathic pain through regulating miR‐448 and JAK1. Issue 10 (3rd February 2020)

• Record Type: Journal Article
• Authors: Wang, Li; Zhu, Kairun; Yang, Bingyi; Cai, Yi
• Is Part Of: Journal of cellular physiology. Volume 235:Issue 10(2020:Oct.)
• Page Start: 6528
• Page End: 6535
• Publication Date: 2020-02-03
• Subjects: JAK1 -- Linc00052 -- miR‐448 -- neuropathic pain; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.29465
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: The dysfunction of the nervous system contributes to neuropathic pain. Long noncoding RNAs are reported to participate in neuropathic pain. Recently, Linc00052 is implicated to be closely associated with multiple diseases. Nevertheless, the mechanisms of Linc00052 remain barely explored in neuropathic pain development. Currently, spinal nerve ligation (SNL) triggered neuropathic pain was employed in our investigation. Here, we assessed the function of Linc00052 in SNL rat models. Interestingly, we reported Linc00052 was significantly elevated in SNL rats. Loss of Linc00052 could reduce neuropathic pain progression via regulating the behaviors of neuropathic pain. Additionally, knockdown of Linc00052 repressed the processes of neuroinflammation. Interleukin (IL)‐6 and tumor necrosis factor α level were inhibited while IL‐10 was induced by the silence of Linc00052. Moreover, we predicted miR‐448 can serve as a target of Linc00052. miR‐448 exerts a crucial power in several diseases. Currently, we exhibited miR‐448 was remarkably downregulated in SNL rats. RNA immunoprecipitation experiments validated the association between miR‐448 and Linc00052. Inhibition of Linc00052 could reverse the roles of miR‐448 on neuropathic pain development. Furthermore, Janus kinase 1 (JAK1) was displayed as the putative target of miR‐448 in the present investigation. It was showed that JAK1 was induced in SNL rats. Loss of miR‐448 could dramatically induce the expression of JAK1, which was rescued by knockdown of Linc00052. Taken these together, our study implied that Linc00052 functioned as a novel target of neuropathic pain via sponging miR‐448 and regulating JAK1. Abstract : We reported that Janus kinase 1 (JAK1) was increased in spinal nerve ligation (SNL) rat models, which was a target of miR‐448. In addition, knockdown of Linc00052 could repress JAK1 via sponging miR‐448. To sum up, our findings revealed Linc00052 contributed to neuropathic pain progression via sponging miR‐448 and regulating JAK1 in SNL model rats.