SNP rs322931 (C>T) in miR-181b and rs7158663 (G>A) in MEG3 aggravate the inflammatory response of anal abscess in patients with Crohn's disease

Aging (Albany NY). 2022 Apr 14;14(7):3313-3324. doi: 10.18632/aging.204014. Epub 2022 Apr 14.

Abstract

Background: The MEG3/miR-181b signaling has been implicated in the pathogenesis of several diseases including Crohn's disease. This work aimed to study the correlation between SNPs in MEG3/miR-181b and the severity of anal abscess in patients with Crohn's disease.

Methods: Quantitative real-time PCR was performed to analyze the expression of MEG3 and miR-181b. ELISA was carried out to examine the expression of TNF-α, IL-1β, IL-6, CRP, SSA, AAT, AAG and HPT in the peripheral blood of patients with Crohn's disease. Luciferase assay was performed to explore the role of miR-181b in the expression of MEG3 and TNF-α.

Results: The expression of MEG3 and miR-181b in the peripheral blood of patients with Crohn's disease was remarkably associated with the rs322931 and rs7158663 polymorphisms. rs322931 (C>T) in miR-181b and rs7158663 (G>A) in MEG3 significantly promoted the expression of TNF-α, IL-1β, IL-6, CRP, SSA, AAT, AAG and HPT. Luciferase assay demonstrated that miR-181b was capable of repressing the expression of MEG3 and TNF-α through binding to their specific binding sites. Moreover, alteration of MEG3 and miR-181b expression also showed a remarkable impact on the MEG3/miR-181b/TNF-α signaling pathway in THP-1 cells.

Conclusions: In conclusion, our study demonstrated that two SNPs, rs322931 (C>T) in miR-181b and rs7158663 (G>A) in MEG3, could aggravate the inflammatory response of anal abscess in patients with Crohn's disease via modulating the MEG3/miR-181b/TNF-α signaling pathway.

Keywords: MEG3; TNF; anal abscess; inflammation; miR-181b.

MeSH terms

  • Abscess* / genetics
  • Anus Diseases* / genetics
  • Crohn Disease* / complications
  • Crohn Disease* / genetics
  • Humans
  • Luciferases
  • MicroRNAs* / genetics
  • Polymorphism, Single Nucleotide
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • MEG3 non-coding RNA, human
  • MIrn181 microRNA, human
  • MicroRNAs
  • RNA, Long Noncoding
  • Tumor Necrosis Factor-alpha
  • Luciferases