Selenoprotein S is a marker but not a regulator of endoplasmic reticulum stress in intestinal epithelial cells

Speckmann, Bodo, Gerloff, Kirsten, Simms, Lisa, Oancea, Iulia, Shi, Wei, McGuckin, Michael A., Radford-Smith, Graham and Khanna, Kum Kum (2014) Selenoprotein S is a marker but not a regulator of endoplasmic reticulum stress in intestinal epithelial cells. Free Radical Biology and Medicine, 67 265-277. doi:10.1016/j.freeradbiomed.2013.11.001

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Author Speckmann, Bodo
Gerloff, Kirsten
Simms, Lisa
Oancea, Iulia
Shi, Wei
McGuckin, Michael A.
Radford-Smith, Graham
Khanna, Kum Kum
Title Selenoprotein S is a marker but not a regulator of endoplasmic reticulum stress in intestinal epithelial cells
Journal name Free Radical Biology and Medicine   Check publisher's open access policy
ISSN 0891-5849
Publication date 2014-01-01
Year available 2013
Sub-type Article (original research)
DOI 10.1016/j.freeradbiomed.2013.11.001
Open Access Status Not yet assessed
Volume 67
Start page 265
End page 277
Total pages 13
Place of publication Philadelphia, PA United States
Publisher Elsevier Inc.
Language eng
Subject 1303 Specialist Studies in Education
2737 Physiology (medical)
Abstract Selenoproteins are candidate mediators of selenium-dependent protection against tumorigenesis and inflammation in the gut. Expression and roles of only a limited number of intestinal selenoproteins have been described so far. Selenoprotein S (SelS) has been linked to various inflammatory diseases and is suggested to be involved in endoplasmic reticulum (ER) homeostasis regulation and antioxidative protection in a cell-type-dependent manner, but its protein expression, regulation, and function in the gut are not known. We here analyzed the expression and localization of SelS in the healthy and inflamed gut and studied its regulation and function in intestinal epithelial cell lines. SelS was expressed in the intestinal epithelium of the small and large intestine and colocalized with markers of Paneth cells and macrophages. It was upregulated in inflamed ileal tissue from Crohn's disease patients and in two models of experimental colitis in mice. We detected SelS in colorectal cell lines, where it colocalized with the ER marker calnexin. SelS protein expression was unaffected by enterocytic differentiation but increased in response to selenium supplementation and after treatment with the ER stress inducer tunicamycin. On the other hand, depletion of SelS in LS174T, HT29, and Caco-2 cells by RNA interference did not cause or modulate ER stress and had no effect on hydrogen peroxide-induced cell death. In summary, we introduce SelS as a novel marker of Paneth cells and intestinal ER stress. Although it is upregulated in Crohn's disease, its role in disease etiology remains to be established.
Keyword Colitis
Crohn's disease
ER stress
Free radicals
Q-Index Code C1
Q-Index Status Confirmed Code
Grant ID SP 1333/1-2
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2014 Collection
School of Medicine Publications
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