Connexin expression pattern in the endometrium of baboons is influenced by hormonal changes and the presence of endometriotic lesions

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Connexin expression in baboon endometrium changes with hormonal cycles, and endometriotic lesions further alter this pattern, particularly affecting Cx26, suggesting an impaired implantation process and potential contribution to infertility.

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AI-generated deep summary by claude@2026-06, 2026-06-07

The study examined connexin gene expression in the endometrium of cycling and experimentally endometriosis-induced baboons, focusing on how hormonal phase and the presence of endometriotic lesions alter connexin patterns. In cycling animals, connexin expression resembled human endometrium, with Cx43 mainly in stromal cells and Cx26 and Cx32 predominantly in epithelium; during the secretory phase, Cx32 increased whereas Cx26 and Cx43 decreased. In the induced endometriosis model, the authors observed a lesion-associated shift in the secretory phase in which Cx26 and Cx32 were no longer in the epithelium and Cx26 was instead primarily in stromal cells, and chorionic gonadotrophin infusion failed to rescue the aberrant stromal Cx26 expression. This paper is centrally about endometriosis—specifically, lesion-driven alterations in endometrial connexin expression patterns in a baboon model.

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Abstract

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.

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Condition tags

endometriosisinfertility

MeSH descriptors

Connexins Endometriosis Endometrium Animals Chorionic Gonadotropin Chorionic Gonadotropin Connexin 26 Connexin 43 Connexin 43 Connexins Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Immunohistochemistry Menstrual Cycle Menstrual Cycle Microscopy, Electron, Transmission

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europepmc
last seen: 2026-06-16T06:07:01.518242+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:13:59.677786+00:00
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