Expression pattern of GPR30 in endometriosis

EP Samartzis, N Samartzis, Aurelia Noske, André Fedier, Rosmarie Caduff, D J Fink, P Imesch
In: Geburtshilfe und Frauenheilkunde · 2011 · vol. 71(05) · doi:10.1055/s-0031-1280499 · W2329374199
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This study investigated the expression pattern of G-protein coupled receptor 30 (GPR30) in endometriosis due to its role in estrogen action and proliferative effects.

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Abstract

Introduction: G-protein coupled receptor 30 (GPR30) is a seven-transmembrane receptor suggested to be part of non-genomic estrogen responses that can, in contrast to the classic or genomic mode of ER action, occur rapidly within minutes. GPR30 mediated estrogen action is involved in multiple physiological processes, as well as pathological processes, as for example the proliferative effects of estrogen and tamoxifen in endometrial cancer cells. Since Estrogen action plays a key role in endometriosis and is partly mediated by GPR30 in a various number of physiological and pathological processes, the investigation of its expression in endometriosis could be of particular interest.
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Introduction

G-protein coupled receptor 30 (GPR30) is a seven-transmembrane receptor suggested to be part of non-genomic estrogen responses that can, in contrast to the classic or genomic mode of ER action, occur rapidly within minutes. GPR30 mediated estrogen action is involved in multiple physiological processes, as well as pathological processes, as for example the proliferative effects of estrogen and tamoxifen in endometrial cancer cells. Since Estrogen action plays a key role in endometriosis and is partly mediated by GPR30 in a various number of physiological and pathological processes, the investigation of its expression in endometriosis could be of particular interest.

Methods

Immunohistochemical analysis for GPR30, ER-alpha, ER-beta and PR was performed on a tissue microarray including 74 endometriotic tissue samples of premenopausal women with following localisations (27 ovarian, 19 peritoneal, 28 deep infiltrating lesions). 30 samples of eutopic endometrial tissue served as a control in the same TMA.

Results

High cytoplasmic GPR30 expression was found in 50% (n=30/60) of endometriotic epithelial cells, but in none (0/30) of the eutopic endometrial epithelial cells (p<0.001). Furthermore cytoplasmic GPR30 was expressed significantly stronger in ovarian endometriosis (6/20, 70%; p=0.01) than in peritoneal (9/18, 50%) and deep infiltrating endometriosis (15/22, 31.8%). Nuclear GPR30 expression did not show a significant difference in endometrial lesion to normal endometrium.

Conclusion

Nongenomic GPR30 is known to be part of a signaling pathway inducing cell proliferation and migration. Its overexpression in endometriotic lesion could play an additional role in the hormonal regulation of endometriosis an could represent a novel therapeutical target.

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endometriosis

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