Role of intestinal Hsp70 in barrier maintenance: contribution of milk to the induction of Hsp70.2

Role of intestinal Hsp70 in barrier maintenance: contribution of milk to the induction of Hsp70.2 Background Necrotizing enterocolitis (NEC) is a gastrointestinal disease of complex etiology resulting in devastating sys- temic inflammation and often death in premature newborns. We previously demonstrated that formula feeding inhibits ileal expression of heat shock protein-70 (Hsp70), a critical stress protein within the intestine. Barrier function for the prema- ture intestine is critical. We sought to determine whether reduced Hsp70 protein expression increases neonatal intestinal permeability. Methods Young adult mouse colon cells (YAMC) were utilized to evaluate barrier function as well as intestine from Hsp70−/− pups (KO). Sections of intestine were analyzed by Western blot, immunohistochemistry, and real time PCR. YAMC cells were sub-lethally heated or treated with expressed milk (EM) to induce Hsp70. Results Immunostaining demonstrates co-localized Hsp70 and tight junction protein zona occludens-1 (ZO-1), suggesting physical interaction to protect tight junction function. The permeability of YAMC monolayers increases following oxidant injury and is partially blocked by Hsp70 induction either by prior heat stress or EM. RT-PCR analysis demonstrated that the Hsp70 isoforms, 70.1 and 70.3, predominate in WT pup; however, Hsp70.2 predominates in the KO pups. While Hsp70 is present in WT milk, it is not present in KO EM. Hsp70 associates with ZO-1 to maintain epithelial http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pediatric Surgery International Springer Journals

Role of intestinal Hsp70 in barrier maintenance: contribution of milk to the induction of Hsp70.2

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Publisher
Springer Journals
Copyright
Copyright © 2017 by Springer-Verlag GmbH Germany, part of Springer Nature
Subject
Medicine & Public Health; Pediatrics; Surgery; Pediatric Surgery
ISSN
0179-0358
eISSN
1437-9813
D.O.I.
10.1007/s00383-017-4211-3
Publisher site
See Article on Publisher Site

Abstract

Background Necrotizing enterocolitis (NEC) is a gastrointestinal disease of complex etiology resulting in devastating sys- temic inflammation and often death in premature newborns. We previously demonstrated that formula feeding inhibits ileal expression of heat shock protein-70 (Hsp70), a critical stress protein within the intestine. Barrier function for the prema- ture intestine is critical. We sought to determine whether reduced Hsp70 protein expression increases neonatal intestinal permeability. Methods Young adult mouse colon cells (YAMC) were utilized to evaluate barrier function as well as intestine from Hsp70−/− pups (KO). Sections of intestine were analyzed by Western blot, immunohistochemistry, and real time PCR. YAMC cells were sub-lethally heated or treated with expressed milk (EM) to induce Hsp70. Results Immunostaining demonstrates co-localized Hsp70 and tight junction protein zona occludens-1 (ZO-1), suggesting physical interaction to protect tight junction function. The permeability of YAMC monolayers increases following oxidant injury and is partially blocked by Hsp70 induction either by prior heat stress or EM. RT-PCR analysis demonstrated that the Hsp70 isoforms, 70.1 and 70.3, predominate in WT pup; however, Hsp70.2 predominates in the KO pups. While Hsp70 is present in WT milk, it is not present in KO EM. Hsp70 associates with ZO-1 to maintain epithelial

Journal

Pediatric Surgery InternationalSpringer Journals

Published: Dec 1, 2017

References

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