Mol. Hum. Reprod. Advance Access originally published online on August 6, 2009
Molecular Human Reproduction 2009 15(10):645-652; doi:10.1093/molehr/gap060
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This article appears in the following Molecular Human Reproduction issue: Special Issue: Mechanisms of Endometriosis [View the issue table of contents]
Connexin expression pattern in the endometrium of baboons is influenced by hormonal changes and the presence of endometriotic lesions
1Institute of Molecular Biology, University of Duisburg-Essen, 45122 Essen, Germany 2Department of Obstetrics and Gynaecology, University of Illinois at Chicago, Chicago, IL 60612, USA 3Maternal and Fetal Health Research Group, University of Manchester, St Mary's Hospital, Manchester, UK 4MRC Human Reproductive Sciences Unit, Queen's Medical Research Institute, Edinburgh, UK
5 Correspondence address. Tel: +49-2017234387; Fax: +49-2017235974; E-mail: elke.winterhager{at}uk-essen.de
Experimentally induced endometriosis in baboons serves as an elegant model to discriminate between endometrial genes which are primarily associated with normal endometrial function and those that are changed by the presence of endometriotic lesions. Since connexin genes are characteristic of the hormonally regulated differentiation of the endometrium, we have examined connexin expression in baboon endometrium to delineate if they are altered in response to the presence of endometriotic lesions. Connexin expression in the endometrium of cycling baboons is similar to that of the human endometrium with Connexin(Cx)43 being primarily seen in the stromal compartment and Cx26 and Cx32 being present predominantly in the epithelium. Although Cx32 is up-regulated during the secretory phase, Cx26 and Cx43 are down-regulated. In the baboon model of induced endometriosis a change in connexin pattern was evident in the presence of endometriotic lesions. In the secretory phase, Cx26 and Cx32 are no longer present in the epithelium but Cx26 is now observed primarily in the stromal cells. Infusion of chorionic gonadotrophin in a manner that mimics blastocyst transit in utero failed to rescue the aberrant stromal expression of Cx26 that is associated with the presence of endometriotic lesions suggesting an impairment of the implantation process. The altered connexin pattern coupled with a loss of the channel protein in the epithelium and a gain of Cx26 in the stromal compartment suggests that the presence of lesions changes the uterine environment and thereby the differentiation programme. This aberrant expression of connexins may be an additional factor that contributes to endometriosis-associated infertility.
Key words: baboon/chorionic gonadotrophin/connexin26/connexin43/endometriosis
Submitted on June 19, 2009; resubmitted on July 15, 2009; accepted on July 22, 2009.