Research Papers:

Loss of epithelium-specific GPx2 results in aberrant cell fate decisions during intestinal differentiation

Claudia Lennicke, Jette Rahn, Claudia Wickenhauser, Rudolf Lichtenfels, Andreas S. Müller, Ludger A. Wessjohann, Anna P. Kipp and Barbara Seliger _

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Oncotarget. 2018; 9:539-552. https://doi.org/10.18632/oncotarget.22640

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Claudia Lennicke1, Jette Rahn1, Claudia Wickenhauser2, Rudolf Lichtenfels1, Andreas S. Müller3, Ludger A. Wessjohann4, Anna P. Kipp5 and Barbara Seliger1

1Institute of Medical Immunology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany

2Institute of Pathology, Martin Luther University Halle-Wittenberg, 06112 Halle (Saale), Germany

3Delacon Biotechnik GmbH, 4221 Steyregg, Austria

4Department of Bioorganic Chemistry, Leibniz-Institute of Plant Biochemistry, 06120 Halle (Saale), Germany

5Institute of Nutrition, Friedrich Schiller University Jena, 07743 Jena, Germany

Correspondence to:

Barbara Seliger, email: [email protected]

Keywords: glutathione peroxidase 2; selenium; DIGE; stem cells; Clca1

Received: May 25, 2017     Accepted: October 27, 2017     Published: November 23, 2017


The selenoprotein glutathione peroxidase 2 (GPx2) is expressed in the epithelium of the gastrointestinal tract, where it is thought to be involved in maintaining mucosal homeostasis. To gain novel insights into the role of GPx2, proteomic profiles of colonic tissues either derived from wild type (WT) or GPx2 knockout (KO) mice, maintained under selenium (Se) deficiency or adequate Se supplementation conditions were established and analyzed. Amongst the panel of differentially expressed proteins, the calcium-activated chloride channel regulator 1 (CLCA1) was significantly down-regulated in GPx2 KO versus WT mice regardless of the given Se status. Moreover, transcript levels of the isoforms CLCA2 and CLCA3 showed a similar expression pattern. In the intestine, CLCA1 is usually restricted to mucin-producing goblet cells. However, although -SeKO mice had the highest numbers of goblet cells as confirmed by significantly enhanced mRNA expression levels of the goblet cell marker mucin-2, the observed expression pattern suggests that GPx2 KO goblet cells might be limited in synthesizing CLCA1. Furthermore, transcript levels of differentiation markers such as chromogranin-1 (Chga) for enteroendocrine cells and leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5) for stem cells were also downregulated in GPx2 KO mice. Moreover, this was accompanied by a downregulation of the mRNA expression levels of the intestinal hormones glucagon-like peptide 1 (Glp1), ghrelin (Ghrl) and somatostatin (Sst). Thus, it seems that GPx2 might be important for the modulation of cell fate decisions in the murine intestinal epithelium.

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