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Novel In Vivo Micro-Computed Tomography Imaging Techniques for Assessing the Progression of Non-Alcoholic Fatty Liver Disease
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Colon Epithelial MicroRNA Network in Fatty Liver

Paule V Joseph1, Sarah K Abey1, Dan Wang1

  • 1Digestive Disorder Unit, Division of Intramural Research, National Institute of Nursing Research, National Institutes of Health, Bethesda, MD 20892, USA.

Canadian Journal of Gastroenterology & Hepatology
|October 23, 2018
PubMed
Abstract

Insights

This study reveals a microRNA (miR) network in colorectal cells linked to fatty liver and metabolic syndrome. The findings highlight how specific miRs impact intestinal barrier function and cell junctions, offering insights into disease mechanisms.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Metabolic Diseases

Background:

  • Intestinal barrier dysfunction is linked to fatty liver (FL) and metabolic syndrome (MetS).
  • MicroRNA (miR) signaling in MetS-FL pathogenesis is not fully understood.
  • This study focuses on an epithelial-centric miR network in colorectal cells.

Purpose of the Study:

  • Investigate the role of a specific trio of miRs (hsa-miR-142-3p, hsa-miR-18b, hsa-miR-890) in MetS-FL.
  • Elucidate the epithelial-focused miR network in colorectal cells.
  • Determine the impact of these miRs on intestinal barrier integrity and cell junctions.

Main Methods:

  • Transfected human colorectal cells (CRL-1790, Caco-2) with MetS-FL miR mimics.
  • Profiled global miRNome changes using NanoString nCounter® Human v3 miRNA.
  • Assessed barrier function (TEER) and epithelial cell junction structure (Occludin, ZO-1).

Main Results:

  • Transfection altered the miRNome, with 288 miRs showing twofold changes.
  • Eleven common miRs with cytoskeletal/metabolic roles were identified.
  • MetS-FL miRs induced TEER variations and altered ZO-1/Occludin structure.
  • A signaling network centered on TNF and AKT2 was revealed, involving injury, inflammation, and hyperplasia.

Conclusions:

  • A colon-specific epithelial barrier and cell junction signaling network was identified.
  • Functional studies of the MetS-FL miR trio signature provide new insights.
  • The findings implicate specific miRs in MetS-FL pathogenesis via intestinal barrier disruption.

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