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The glycosyltransferase EOGT regulates adropin expression in decidualizing human endometrium

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Muter, Joanne, Alam, Mohammad T., Vrljicak, Pavle, Barros, Flavio S. V., Ruane, Peter T., Ewington, Lauren J., Aplin, John D., Westwood, Melissa and Brosens, Jan J. (2018) The glycosyltransferase EOGT regulates adropin expression in decidualizing human endometrium. Endocrinology, 159 (2). pp. 994-1004. doi:10.1210/en.2017-03064 ISSN 0013-7227.

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Official URL: https://doi.org/10.1210/en.2017-03064

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Abstract

In pregnancy, resistance of endometrial decidual cells to stress signals is critical for the integrity of the feto-maternal interface and, by extension, survival of the conceptus. O-GlcNAcylation is an essential post-translational modification that links glucose sensing to cellular stress resistance. Unexpectedly, decidualization of primary endometrial stromal cells (EnSCs) was associated with a 60% reduction in O-GlcNAc modified proteins, reflecting downregulation of the enzyme that adds O-GlcNAc to substrates (O-GlcNAc transferase, OGT) but not the enzyme that removes the modification (O-GlcNAcase, OGA). Notably, EOGT, an endoplasmic reticulum-specific O-GlcNAc transferase that modifies a limited number of secreted and membrane proteins, was markedly induced in differentiating EnSCs. Knockdown of EOGT perturbed a network of decidual genes involved in multiple cellular functions. The most downregulated gene upon EOGT knockdown in decidualizing cells was ENHO, which encodes adropin, a metabolic hormone involved in energy homeostasis and glucose and fatty acid metabolism. Analysis of mid-luteal endometrial biopsies revealed an inverse correlation between endometrial EOGT and ENHO expression and body mass index. Taken together, our findings reveal that obesity impairs the EOGT-adropin axis in decidual cells, which in turn points towards a novel mechanistic link between metabolic disorders and adverse pregnancy outcome. [Abstract copyright: Copyright © 2017 Endocrine Society.]

Item Type: Journal Article
Subjects: Q Science > QP Physiology
R Medicine > RG Gynecology and obstetrics
Divisions: Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Cell & Developmental Biology
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School
SWORD Depositor: Library Publications Router
Library of Congress Subject Headings (LCSH): Endometrium -- physiological aspects, Miscarriage
Journal or Publication Title: Endocrinology
Publisher: Endocrine Society
ISSN: 0013-7227
Official Date: 1 February 2018
Dates:
DateEvent
1 February 2018Published
13 December 2017Available
4 December 2017Accepted
Volume: 159
Number: 2
Page Range: pp. 994-1004
DOI: 10.1210/en.2017-03064
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Restricted or Subscription Access
Date of first compliant deposit: 17 January 2018
Date of first compliant Open Access: 13 December 2018
RIOXX Funder/Project Grant:
Project/Grant IDRIOXX Funder NameFunder ID
15/0005207Diabetes UKhttp://dx.doi.org/10.13039/501100000361
UNSPECIFIEDUniversity Hospitals Coventry and Warwickshire NHS Trusthttps://viaf.org/viaf/152707181
UNSPECIFIEDTommy’s National Centre for Miscarriage ResearchUNSPECIFIED
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