title: Role of peroxisome proliferator-activated receptor-alpha in ileum tight junction alteration in mouse model of restraint stress.
abstract: Restraint stress induces permeability changes in the small intestine, but little is known about the role of endogenous peroxisome proliferator-activated receptor-alpha (PPAR-alpha) ligand in the defects of the tight junction function. In the present study, we used PPAR-alpha knockout mice to understand the roles of endogenous PPAR-alpha on ileum altered permeability function in models of immobilization stress. The absence of a functional PPAR-alpha gene in PPAR-alpha knockout mice resulted in a significant augmentation of the degree of 1) TNF-alpha production in ileum tissues; 2) the alteration of zonula occludens-1, occludin, and beta-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-alpha ligands reduce the degree of tight junction permeability in the ileum tissues associated with immobilization stress, suggesting a possible role of endogenous PPAR-alpha ligands on ileum barrier dysfunction.
authors: Istituto di Ricovero e Cura a Carattere Scientifico Centro Neurolesi Bonino-Pulejo, Messina, Italy.
authors: Emanuela
authors: E
authors: Mazzon
authors: Concetta
authors: C
authors: Crisafulli
authors: Maria
authors: M
authors: Galuppo
authors: Salvatore
authors: S
authors: Cuzzocrea
mesh_terms: D000818:Animals; D017209:Apoptosis; D003106:Colon / Q000378:metabolism; D003672:Defecation; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000378:metabolism; D004847:Epithelial Cells / Q000378:metabolism; D053222:Fas Ligand Protein / Q000378:metabolism; D007082:Ileum / Q000378:metabolism* / Q000648:ultrastructure; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000648:ultrastructure; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D062793:Occludin; D047493:PPAR alpha / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D010539:Permeability; D010750:Phosphoproteins / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012149:Restraint, Physical; D013315:Stress, Psychological / Q000378:metabolism* / Q000473:pathology; D019108:Tight Junctions / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D062826:Zonula Occludens-1 Protein; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D051176:beta Catenin / Q000378:metabolism
chemical_list: C494827:Bax protein, mouse; C495267:CTNNB1 protein, mouse; D053222:Fas Ligand Protein; D008565:Membrane Proteins; D062793:Occludin; C568986:Ocln protein, mouse; D047493:PPAR alpha; D010750:Phosphoproteins; D019253:Proto-Oncogene Proteins c-bcl-2; C569043:Tjp1 protein, mouse; D014409:Tumor Necrosis Factor-alpha; D062826:Zonula Occludens-1 Protein; D051028:bcl-2-Associated X Protein; D051176:beta Catenin