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MicroRNA 29 targets nuclear factor-κB-repressing factor and Claudin 1 to increase intestinal permeability

QiQi Zhou1, Stefan Costinean2, Carlo M Croce2

  • 1Department of Medicine, University of Texas Medical Branch, Galveston, Texas; Department of Veteran Affairs, Cincinnati VA Medical Center, Cincinnati, Ohio.

Gastroenterology
|October 4, 2014
PubMed
Abstract

Insights

MicroRNA 29 (MIR29) increases intestinal permeability in irritable bowel syndrome with diarrhea (IBS-D) by reducing Claudin-1 and NKRF. Blocking MIR29 may restore gut barrier function in IBS-D patients.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Genetics

Background:

  • Irritable bowel syndrome with diarrhea (IBS-D) is associated with intestinal hyperpermeability.
  • MicroRNA 29 (MIR29) plays a role in regulating intestinal permeability in IBS-D patients.

Purpose of the Study:

  • To investigate the targets of MIR29.
  • To examine the effects of Mir29 disruption on intestinal permeability in a mouse model.

Main Methods:

  • Expression analysis of MIR29A/B in intestinal biopsies from IBS patients and controls.
  • Generation and study of Mir29 knockout mice, including induction of colitis and assessment of intestinal permeability.
  • Microarray analysis and knockdown experiments in human intestinal cell lines.

Main Results:

  • Patients with IBS-D showed increased MIR29A/B and decreased Claudin-1 (CLDN1) and nuclear factor-κB-repressing factor (NKRF) levels.
  • Mir29 knockout mice exhibited reduced intestinal permeability following colitis induction compared to wild-type mice.
  • MIR29A/B were found to reduce NKRF and CLDN1 mRNA levels, impacting intestinal permeability.

Conclusions:

  • MIR29 targets CLDN1 and NKRF, increasing intestinal permeability in IBS-D.
  • Therapeutic strategies aimed at blocking MIR29 could potentially restore intestinal barrier function in IBS-D.
Keywords:
Gene RegulationIntestinal Barrier FunctionMouse ModelmRNA Processing

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