Role of peroxisome proliferator-activated receptor-α in ileum tight junction alteration in mouse model of restraint stress

Emanuela Mazzon, Concetta Crisafulli, Maria Galuppo, Salvatore Cuzzocrea

Research output: Contribution to journalArticlepeer-review

Abstract

Restraint stress induces permeability changes in the small intestine, but little is known about the role of endogenous peroxisome proliferator-activated receptor-α (PPAR-α) ligand in the defects of the tight junction function. In the present study, we used PPAR-α knockout mice to understand the roles of endogenous PPAR-α on ileum altered permeability function in models of immobilization stress. The absence of a functional PPAR-α gene in PPAR-α knockout mice resulted in a significant augmentation of the degree of 1) TNF-α production in ileum tissues; 2) the alteration of zonula occludens-1, occludin, and β-catenin (immunohistochemistry); and 3) apoptosis (terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling staining, Bax, Bcl-2 expression). Taken together, our results demonstrate that endogenous PPAR-α ligands reduce the degree of tight junction permeability in the ileum tissues associated with immobilization stress, suggesting a possible role of endogenous PPAR-α ligands on ileum barrier dysfunction.

Original languageEnglish
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume297
Issue number3
DOIs
Publication statusPublished - Sep 2009

Keywords

  • β-catenin
  • Apoptosis
  • Occludin
  • Peroxisome proliferator-activated receptor-α-deficient mice
  • Zonula occludens-1

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology
  • Hepatology
  • Physiology (medical)

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