Zinc induces hephaestin expression via a PI3K-CDX2 dependent mechanism to regulate iron transport in intestinal Caco-2 cells.

Autor: Ramavath HN; Drug Safety Division, ICMR-National Institute of Nutrition, Hyderabad, India., Chandra Mashurabad P; Drug Safety Division, ICMR-National Institute of Nutrition, Hyderabad, India., Yaduvanshi PS; Drug Safety Division, ICMR-National Institute of Nutrition, Hyderabad, India., Veleri S; Drug Safety Division, ICMR-National Institute of Nutrition, Hyderabad, India., Sharp PA; Department of Nutritional Sciences, Kings College London, UK., Pullakhandam R; Drug Safety Division, ICMR-National Institute of Nutrition, Hyderabad, India. Electronic address: raghu_nin2000@yahoo.com.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2022 Oct 20; Vol. 626, pp. 1-7. Date of Electronic Publication: 2022 Jul 30.
DOI: 10.1016/j.bbrc.2022.07.053
Abstrakt: Zinc stimulates intestinal iron absorption via induction of divalent metal ion transporter (DMT1) and hephaestin (HEPH). While the increase in DMT1 is mediated via a PI3K/IPR2 axis, the mechanisms of Zn-induced HEPH expression downstream of PI3K remain elusive. In the current study we probed the role of Caudal-related homeobox transcription factor-2 (CDX2) on Zn-induced HEPH expression. Zn treatment of Caco-2 cells increased CDX2 phosphorylation and HEPH protein and mRNA expression. siRNA-silencing of CDX2 inhibited Zn-induced HEPH expression. LY294002, an antagonist of PI3K inhibited Zn-induced phosphorylation of CDX2, and downstream HEPH expression. These results suggest that increased expression of HEPH in intestinal cells following Zn treatment is mediated via a PI3K-CDX2 pathway.
Competing Interests: Declaration of conflict of interest The authors declare no conflict of interest.
(Copyright © 2022 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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