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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 9674272, 7 pages
http://dx.doi.org/10.1155/2016/9674272
Research Article

Reinforced Epithelial Barrier Integrity via Matriptase Induction with Sphingosine-1-Phosphate Did Not Result in Disturbances in Physiological Redox Status

1Department of Pharmacology and Toxicology, Faculty of Veterinary Science, Szent István University, István u. 2, Budapest 1078, Hungary
21st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői ut 26, Budapest 1085, Hungary
3Faculty of Pharmacy, Semmelweis University, Hőgyes u. 7, Budapest 1092, Hungary
4Agro-Environmental Research Institute, National Agricultural Research and Innovation Centre, Herman O. u. 15, Budapest 1022, Hungary

Received 17 June 2015; Revised 10 October 2015; Accepted 19 October 2015

Academic Editor: Silvana Hrelia

Copyright © 2016 E. Pászti-Gere et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objectives. The relationship among matriptase function, cellular redox status, and maintenance of intestinal barrier integrity has not been established yet. The aim of this study is to reveal if the crosstalk between matriptase activators and intestinal epithelial monolayers can lead to perturbations in physiological redox regulation in vitro. Methods. The effects of suramin and sphingosine-1-phosphate (S1P) were tested on viability of intestinal porcine epithelial IPEC-J2 cells using MTS assay. Measurements of transepithelial electrical resistance (TER) were performed to determine changes in barrier integrity of cell monolayers. Amplex Red assay was used to monitor extracellular hydrogen peroxide production. Occludin distribution pattern was detected prior to and after matriptase activation using immunofluorescent staining technique. Results. TER reduction was observed in suramin-treated IPEC-J2 cell monolayers, which could be attributed to cell cytotoxic properties of 48 hr 50 μM suramin administration. In contrast, S1P treatment increased TER significantly and elevated occludin accumulation in tight junctions. It was also found that extracellular hydrogen peroxide levels were maintained in IPEC-J2 cells exposed to matriptase activators. Discussion. S1P administration not accompanied by redox imbalance might be one of the key strategies in the improvement of barrier function and consequently in the therapy of intestinal inflammations.