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Murine Model of Intestinal Ischemia-reperfusion Injury
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Murine Model of Intestinal Ischemia-reperfusion Injury

Published on: May 11, 2016

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Inhibition of miR-142-3p promotes intestinal epithelial proliferation and barrier function after ischemia/reperfusion

Yuhang Wang1,2, Zirui Jia1,2, Mingcan Zheng1,2

  • 1Department of Gastroenterology Surgery, the Central Hospital of Dalian University of Technology (Dalian Municipal Central Hospital), No. 826 of Southwest Road Shahekou District, Dalian, 116033, People's Republic of China.

Molecular and Cellular Biochemistry
|May 31, 2024
PubMed

Insights

MicroRNA-142 (miR-142) increases after intestinal ischemia/reperfusion (I/R) injury, impairing barrier function. Inhibiting miR-142 enhances intestinal epithelial proliferation and barrier function, improving survival rates.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Intestinal ischemia/reperfusion (I/R) injury severely damages intestinal barrier function (BF), leading to high mortality.
  • MicroRNAs (miRNAs) are implicated in regulating intestinal mucosal BF and epithelial proliferation post-I/R.
  • Understanding the specific roles of miRNAs in I/R injury is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the role and regulatory mechanism of miR-142-3p (miR-142) in intestinal epithelial proliferation and BF following I/R injury.
  • To determine if miR-142 directly targets key regulatory molecules involved in intestinal repair.
  • To assess the therapeutic potential of modulating miR-142 in I/R injury models.

Main Methods:

  • Analysis of miR-142 expression, proliferation, and BF in clinical ischemic intestinal tissues.
  • Establishment of in vivo (mouse I/R) and in vitro (IEC-6 cell hypoxia/reoxygenation) models.
  • Manipulation of miR-142 expression levels to evaluate its impact on intestinal epithelial cells and survival rates.
  • Bioinformatics analysis and luciferase assays to identify direct miR-142 targets.

Main Results:

  • miR-142 expression was significantly elevated in clinical and experimental I/R-injured intestinal tissues.
  • Increased miR-142 inversely correlated with intestinal epithelial proliferation and BF.
  • Inhibition of miR-142 markedly enhanced intestinal epithelial proliferation and BF post-I/R injury.
  • miR-142 directly targets Forkhead box M1 (FoxM1), a key regulator of cell proliferation.
  • Blocking miR-142 improved the survival rate of mice subjected to I/R injury.

Conclusions:

  • miR-142 plays a detrimental role in intestinal epithelial proliferation and BF after I/R injury.
  • Inhibition of miR-142 represents a promising therapeutic strategy for I/R injury by promoting intestinal repair via FoxM1.
  • Targeting miR-142 offers a novel approach to improve outcomes in patients suffering from intestinal I/R injury.
Keywords:
Barrier functionFoxM1IntestineIschemia/reperfusion injuryProliferationmiR-142-3p

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