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EphrinA1/EphA2 Promotes Epithelial Hyperpermeability Involving in Lipopolysaccharide-induced Intestinal Barrier

Yuhua Chen1, Lei Zhang1, Yongbo Zhang1,2

  • 1Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Journal of Neurogastroenterology and Motility
|July 2, 2020
PubMed
Summary
This summary is machine-generated.

Lipopolysaccharide (LPS) disrupts intestinal barrier function. The EphrinA1/ephA2 pathway, via ERK1/2, exacerbates this LPS-induced hyperpermeability, highlighting a therapeutic target.

Keywords:
EphA2FcLipopolysaccharidesReceptorTight junction proteins

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Area of Science:

  • Cell biology
  • Immunology
  • Gastroenterology

Background:

  • Lipopolysaccharide (LPS) is a primary inducer of mucosal and systemic inflammation, compromising epithelial barrier integrity in various diseases.
  • The EphrinA1/ephA2 signaling pathway is implicated in regulating epithelial permeability through cell-cell interactions.

Purpose of the Study:

  • To investigate the specific role of the EphrinA1/ephA2 pathway in lipopolysaccharide (LPS)-induced epithelial hyperpermeability.
  • To elucidate the molecular mechanisms underlying EphrinA1/ephA2 involvement in intestinal barrier dysfunction.

Main Methods:

  • Established in vivo (oral LPS in mice) and in vitro (LPS-treated Caco2 cells) models to assess epithelial barrier function.
  • Evaluated tight junction proteins (occludin, claudin-1), transepithelial electrical resistance, and macromolecule permeability (FD4).
  • Quantified EphrinA1/ephA2 expression and phosphorylation, and modulated pathway activity using ephrinA1-Fc, ephA2-Fc, ephA2-mab, and ERK1/2 inhibitor (PD98059).

Main Results:

  • LPS induced significant barrier dysfunction, characterized by reduced tight junction protein expression, decreased electrical resistance, and increased permeability.
  • LPS upregulated the EphrinA1/ephA2 pathway and ephA2 phosphorylation; blocking ephA2 or inhibiting ERK1/2 ameliorated LPS-induced hyperpermeability.
  • EphrinA1 stimulation promoted epithelial leakage via ERK1/2 phosphorylation, which was reversed by ephA2 inhibition and PD98059.

Conclusions:

  • The EphrinA1/ephA2 pathway significantly contributes to epithelial hyperpermeability.
  • This pathway operates via an ERK1/2-dependent mechanism in the context of LPS-induced intestinal barrier dysfunction.
  • Targeting the EphrinA1/ephA2/ERK1/2 axis may offer a therapeutic strategy for inflammatory conditions involving intestinal barrier disruption.