HOXB13 induced LncRNA CYTOR aggravates spinal cord injury induced neuropathic pain via upregulating TJP1

Abstract Neuropathic pain (NP) is characterized as a pain disorder results from a lesion or disease of the nervous system. Due to the NP is related to multiple disease development including Shingles, stroke, cancer, trauma, and orthopedics, the prevalence of NP has reach to 10% all over the world. However, the underlying molecular mechanisms of NP progression remains unclear. Studies have reported that lncRNA is closely related to NP progression. In this study, we aimed to identify a novel functional lncRNA in NP. Firstly, our study successfully constructed chronic constructive injury (CCI) rat models for NP study. By performing lncRNA microarray analysis, we found that lncRNA CYTOR was markedly upregulated in the CCI rats. Subsequently, we performed a serial experiment to understanding the function of CYTOR in NP. Biologically, our results suggest that CYTOR aggravates NP progression and influences inflammation factors level in nerve tissues of CCI rats. Mechanically, our data indicate that CYTOR, transcriptionally regulated by HOXB13, upregulates TJP1 expression through sponging miR-105-5p. Our study identified a novel functional lncRNA CYTOR in NP progression, which might provide new insights for developing more effective diagnosis or therapeutic strategies for NP.