Inducers of G-protein coupled estrogen receptor (GPER) in endometriosis: potential implications for macrophages and follicle maturation

Heublein S, Sabine Heublein, Thomas Vrekoussis, Vrekoussis T, Kuhn C, Christina Kuhn, Christina Kühn, Friese K, Klaus Friese, Antonis Makrigiannakis, Doris Mayr, Mayr D, Miriam Lenhard, Lenhard M, Jeschke U, Udo Jeschke
Journal of Reproductive Immunology · 2013 · vol. 97(1) , pp. 95–103 · doi:10.1016/j.jri.2012.10.013 · PMID:23432876 · W1985106010
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This paper investigates compounds that activate GPER, exploring their potential roles in regulating macrophages and supporting follicle maturation, particularly in the context of endometriosis.

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Abstract

Endometriosis is an estrogen dependent chronic inflammation and thus a condition of stress. Though the G-protein coupled estrogen receptor (GPER) has been shown to be up-regulated in ovarian endometriosis, insights involved in inducing this receptor expression are largely elusive. Therefore, this study investigated whether stress-related factors (ACTH, prednisolone) or inflammatory factors (IL-1β, TNFα, and PGE(2)) factors may affect GPER. To further link GPER to endometriosis pathophysiology it was tracked in macrophages and follicles of endometriotic ovaries. This study found GPER expression to be modulated by stress-related hormones as well as inflammation and to be up-regulated in endometriosis-associated macrophages. At the same time, follicles of ovaries affected by endometriosis presented significantly reduced GPER positivity when compared to controls, suggesting a possible way by which endometriosis may affect folliculogenesis. The multiple roles of GPER as presented herein make it a promising future candidate for targeted molecular endometriosis treatment.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Inflammation Receptors, Estrogen Receptors, G-Protein-Coupled Stress, Psychological Adrenocorticotropic Hormone Adrenocorticotropic Hormone Adrenocorticotropic Hormone Adult Cell Line, Tumor Dinoprostone Dinoprostone Dinoprostone Endometriosis Endometriosis Endometrium Endometrium Female Gene Expression Regulation

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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Cited by (14)

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License: CC0 · commercial use OK