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NADPH oxidase-derived reactive oxygen species mediate decidualization of human endometrial stromal cells in response to cyclic AMP signaling

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Al-Sabbagh, M., Fusi, L., Higham, J., Lee, Y., Lei, K., Hanyaloglu, A. C., Lam, E. W.- F., Christian, Mark and Brosens, Jan J. (2011) NADPH oxidase-derived reactive oxygen species mediate decidualization of human endometrial stromal cells in response to cyclic AMP signaling. Endocrinology, Vol.152 (No.2). pp. 730-740. doi:10.1210/en.2010-0899 ISSN 0013-7227.

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Official URL: http://dx.doi.org/10.1210/en.2010-0899

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Abstract

Differentiation of human endometrial stromal cells into specialized decidual cells is critical for embryo implantation and survival of the conceptus. Initiation of this differentiation process is strictly dependent on elevated cAMP levels, but the signal intermediates that control the expression of decidual marker genes, such as prolactin (PRL) and IGFBP1, remain poorly characterized. Here we show that cAMP-dependent decidualization can be attenuated or enhanced upon treatment of primary cultures with a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor (diphenylen iodonium) or activator (apocynin), respectively. Time-course analysis demonstrated that cAMP enhances endogenous reactive oxygen species production, apparent after 12 h of stimulation, which coincides with a dramatic increase in decidual PRL and IGFBP1 expression. Knockdown of the Rho GTPase RAC1, which disables activation of the NADPH oxidase homologs NADPH oxidase (NOX)-1, NOX-2, and NOX-3, had no effect on PRL or IGFBP1 expression. In contrast, silencing of NOX-4, or its cofactor p22PHOX, inhibited the expression of both decidual markers. Finally, we show that the NOX-4/p22PHOX complex regulates the DNA-binding activity of CCAAT/enhancer binding protein-β, a key regulator of human endometrial stromal cell differentiation. Thus, NOX-4 activation and reactive oxygen species signaling play an integral role in initiating the endometrial decidual response in preparation of pregnancy.

Item Type: Journal Article
Subjects: R Medicine > R Medicine (General)
Divisions: Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Reproductive Health ( - until July 2016)
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School
Journal or Publication Title: Endocrinology
Publisher: Endocrine Society
ISSN: 0013-7227
Official Date: February 2011
Dates:
DateEvent
February 2011Published
Volume: Vol.152
Number: No.2
Page Range: pp. 730-740
DOI: 10.1210/en.2010-0899
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Restricted or Subscription Access

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