Orso, E. and Moehle, C. and Boettcher, A. and Szakszon, K. and Werner, T. and Langmann, T. and Liebisch, G. and Buechler, C. and Ritter, M. and Kronenberg, F. and Dieplinger, H. and Bornstein, S. R. and Stremmel, W. and Schmitz, G. (2007) The satiety factor apolipoprotein A-IV modulates intestinal epithelial permeability through its interaction with alpha-catenin: Implications for inflammatory bowel diseases. HORMONE AND METABOLIC RESEARCH, 39 (8). pp. 601-611. ISSN 0018-5043,
Full text not available from this repository. (Request a copy)Abstract
Introduction: Apolipoprotein A-IV (apoA-IV), an intestinally and cerebrally synthesized satiety factor and anti-atherogenic plasma apolipoprotein, was recently identified as an anti-inflammatory protein. In order to elucidate whether intestinal apoA-IV exerts similar repair function as its hepatic homologue apolipoprotein A-V (apoA-V), apoA-IV-interactive proteins were searched and in vitro functional studies were performed with apoA-IV overexpressing cells. ApoA-IV was also analyzed in the intestinal mucosa of patients with inflammatory bowel diseases (IBD), together with other genes involved in epithelial junctional integrity. Methods: A yeast-two-hybrid screening was used to identify apoA-IV-interactors. ApoA-IV was overexpressed in Caco-2 and HT-29 mucosal cells for colocalization and in vitro epithelial permeability studies. Mucosal biopsies from quiescent regions of colon transversum and terminal ileum were subjected to DNA-microarray analysis and pathway-related data mining. Results: Four proteins interacting with apoA-IV were identified, including apolipoprotein B-100, alpha(1)-antichymotrypsin, cyclin C, and the cytosolic adaptor alpha-catenin, thus linking apoA-IV to adherens junctions. Overexpression of apoA-IV was paralleled with a differentiated phenotype of intestinal epithelial cells, upregulation of junctional proteins, and decreased paracellular permeability. Colocalization between alpha-catenin and apoA-IV occurred exclusively in junctional complexes. ApoA-IV was downregulated in quiescent mucosal tissues from patients suffering from IBD. In parallel, only a distinct set of junctional genes was dysregulated in non-inflamed regions of IBD gut. Conclusions: ApoA-IV may act as a stabilizer of adherens junctions interacting with alpha-catenin, and is likely involved in the maintenance of junctional integrity. ApoA-IV expression is significantly impaired in IBD mucosa, even in non-inflamed regions.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | FREE-SOLUTION ISOTACHOPHORESIS; ACUTE-PHASE RESPONSE; CELL-LINE CACO-2; BINDING-PROTEIN; APOA-I; PLASMA; GENE; EXPRESSION; AIV; SECRETION; apolipoproteins; catenins; intestinal permeability; junctional integrity; inflammatory bowel disease |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 01 Dec 2020 13:29 |
| Last Modified: | 01 Dec 2020 13:29 |
| URI: | https://pred.uni-regensburg.de/id/eprint/32444 |
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