Estradiol amplifies interleukin-1-induced monocyte chemotactic protein-1 expression by ectopic endometrial cells of women with endometriosis

Ali Akoum, A Akoum, Akoum A, Jolicoeur C, Christine Jolicoeur, C Jolicoeur, A Boucher, Annie Boucher, Boucher A
The Journal of clinical endocrinology and metabolism · 2000 · vol. 85(2) , pp. 896–904 · doi:10.1210/jcem.85.2.6348 · PMID:10690908 · W2139956233
Lab / animal OA: bronze CC0 ⤵ 41 in-corpus citations
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Estradiol amplifies interleukin-1-induced monocyte chemotactic protein-1 expression in ectopic endometrial cells by increasing transcription, suggesting a mechanism for macrophage recruitment in endometriosis.

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Abstract

Endometriosis, one of the most frequently occurring gynecological disorders, is estrogen dependent and is often associated with immunological changes. These include increased macrophage activation and infiltration into the endometriotic implants themselves as well as the peritoneal cavity where the implants often develop. Despite the critical role estrogens play in the development of endometriosis, the biochemical mechanisms of their action remain unclear. In the present study we report that estradiol (E2) enhances endometriotic cell responsiveness to the proinflammatory cytokine interleukin-1beta by up-regulating interleukin-1-induced monocyte chemotactic protein-1 (MCP-1) expression at the level of both protein secretion and messenger ribonucleic acid (mRNA) synthesis, whereas progesterone had no significant effects. According to mRNA half-life experiments, E2 action does not seem to be due to increased MCP-1 mRNA stability but, rather, to a higher level of transcription, as shown by run-on analysis. Interestingly, immunohistochemical analysis of MCP-1 expression in endometriotic tissue showed intense immunostaining in both epithelial glands and stroma regardless of the menstrual cycle phase, which is consistent with the cell culture data and indicates that MCP-1 expression is not subject to cyclic variation. The findings of the present study for the first time provide evidence that E2 up-regulates, although in an indirect way, the expression of a potent chemotactic and activating factor by ectopic endometrial cells, which may occur locally in the inflammatory site and contribute to peritoneal macrophage recruitment and activation, and reveal a new means of E2 action in the pathophysiology of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Chemokine CCL2 Endometriosis Endometrium Estradiol Interleukin-1 Adult Adult Cells, Cultured Cells, Cultured Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Drug Synergism Drug Synergism Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium

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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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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