Involvement of NRON and TUG1 long noncoding RNAs in inflammation and the pathogenesis of EAE.

There is growing evidence that the long noncoding RNAs (lncRNAs) contribute to the pathogenesis of various neurodegenerative diseases such as multiple sclerosis (MS). The role of lncRNAs nuclear repressor of NFAT (NRON) and Taurine up-regulated 1 (TUG1) in the inflammatory processes occurring in the experimental autoimmune encephalomyelitis (EAE) model of MS is yet to be investigated. Transcript levels of and in acute and chronic phases of EAE and cultured macrophages as well as the correlation between and expression with inflammatory cytokines, were evaluated in this study. EAE experimental model was induced in female C57BL/6 mice with subcutaneous injection of MOGCFA. Mice were scored for 28 days and then sacrificed. The expression of lncRNAs and in lumbar spinal cords, activated and controlled macrophages as well as the expression of , , and inflammatory cytokines, were assayed by real-time RT-PCR. The lncRNAs and were significantly down-regulated in lumbar spinal cords tissues in the acute phase of EAE compared to the control group. and were significantly down-regulated in macrophages treated with 10 ng lipopolysaccharide (LPS) compared to the control macrophages. A negative correlation was identified between and expression and IL-1, IL-6, and CDe-3 inflammatory cytokines. The present study demonstrates the dysregulation of lncRNAs TUG1 and NRON in spinal cord tissue lesions of EAE and activated macrophages, pointing to their potential role in the pathogenesis of EAE.