Inhibition of lncRNA NEAT1 suppresses the inflammatory response in IBD by modulating the intestinal epithelial barrier and by exosome-mediated polarization of macrophages

  • Authors:
    • Rui Liu
    • Anliu Tang
    • Xiaoyan Wang
    • Xiong Chen
    • Lian Zhao
    • Zhiming Xiao
    • Shourong Shen
  • View Affiliations

  • Published online on: August 17, 2018     https://doi.org/10.3892/ijmm.2018.3829
  • Pages: 2903-2913
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Inflammatory bowel disease (IBD) is a multifactorial inflammatory disease, and increasing evidence has demonstrated that the mechanism of the pathogenesis of IBD is associated with intestinal epithelial barrier injury. Long non‑coding RNAs (lncRNAs) are a class of transcripts >200 nucleotides in length with limited protein‑coding capability. Nuclear paraspeckle assembly transcript 1 (NEAT1) is a recently identified nuclear‑restricted lncRNA, which localizes in subnuclear structures, termed paraspeckles, and is involved in the immune response in a variety of ways. However, the function of NEAT1 in IBD remains to be fully elucidated. In the present study, reverse transcription‑quantitative polymerase chain reaction assays were performed to determine the expression levels of NEAT1 lncRNA in IBD serum samples and tissues. Furthermore, the effect of NEAT1 on the cell permeability of colon cells was investigated via determination of trans‑epithelial electrical resistance as well as performance of western blot and immunofluorescence assays. In addition, dextran sodium sulfate assays were performed to investigate the effect of downregulation of NEAT1 in IBD of mice. The present study detected the expression levels of NEAT1 in IBD cells and animal models to examine the changes in intestinal epithelial cell permeability following inhibition of the expression of NEAT1. In addition, phenotypic transformation was examined following different treatments in epithelial cells and macrophages. The results suggested that the expression of NEAT1 was high in IBD and was involved in the inflammatory response by regulating the intestinal epithelial barrier and through exosome‑mediated polarization of macrophages. The downregulation of NEAT1 suppressed the inflammatory response by modulating the intestinal epithelial barrier and through exosome‑mediated polarization of macrophages in IBD. The results of the present study revealed a potential strategy of targeting NEAT1 for IBD therapy.
View Figures
View References

Related Articles

Journal Cover

November-2018
Volume 42 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Liu R, Tang A, Wang X, Chen X, Zhao L, Xiao Z and Shen S: Inhibition of lncRNA NEAT1 suppresses the inflammatory response in IBD by modulating the intestinal epithelial barrier and by exosome-mediated polarization of macrophages. Int J Mol Med 42: 2903-2913, 2018
APA
Liu, R., Tang, A., Wang, X., Chen, X., Zhao, L., Xiao, Z., & Shen, S. (2018). Inhibition of lncRNA NEAT1 suppresses the inflammatory response in IBD by modulating the intestinal epithelial barrier and by exosome-mediated polarization of macrophages. International Journal of Molecular Medicine, 42, 2903-2913. https://doi.org/10.3892/ijmm.2018.3829
MLA
Liu, R., Tang, A., Wang, X., Chen, X., Zhao, L., Xiao, Z., Shen, S."Inhibition of lncRNA NEAT1 suppresses the inflammatory response in IBD by modulating the intestinal epithelial barrier and by exosome-mediated polarization of macrophages". International Journal of Molecular Medicine 42.5 (2018): 2903-2913.
Chicago
Liu, R., Tang, A., Wang, X., Chen, X., Zhao, L., Xiao, Z., Shen, S."Inhibition of lncRNA NEAT1 suppresses the inflammatory response in IBD by modulating the intestinal epithelial barrier and by exosome-mediated polarization of macrophages". International Journal of Molecular Medicine 42, no. 5 (2018): 2903-2913. https://doi.org/10.3892/ijmm.2018.3829