Macrophage Migration Inhibitory Factor Is Involved in a Positive Feedback Loop Increasing Aromatase Expression in Endometriosis

Veillat V, Véronique Veillat, Valérie Sengers, Sengers V, Christine N Metz, Metz CN, Thierry Roger, Mathieu Lebœuf, Mathieu Leboeuf, Mailloux J, Jacques Mailloux, Akoum A, Ali Akoum
The American journal of pathology · 2012 · vol. 181(3) , pp. 917–927 · doi:10.1016/j.ajpath.2012.05.018 · PMID:22759564 · W2112521880
article OA: closed CC0 ⤵ 25 in-corpus citations
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This research identifies macrophage migration inhibitory factor as a component of a positive feedback loop that enhances aromatase expression in endometriosis.

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Abstract

Immune-endocrine interplay may play a major role in the pathogenesis of endometriosis. In the present study, we have investigated the interaction between macrophage migration inhibitory factor (MIF), a major pro-inflammatory and growth-promoting factor markedly expressed in active endometriotic lesions, and estradiol (E(2)) in ectopic endometrial cells. Our data showed a significant increase of MIF protein secretion and mRNA expression in endometriotic cells in response to E(2). MIF production was blocked by Fulvestrant, an estrogen receptor (ER) antagonist, and induced by ERα and ERβ selective agonists propyl-pyrazole-triol (PPT) and diarylpropionrile (DPN), respectively, thus demonstrating a specific receptor-mediated effect. Cell transfection with MIF promoter construct showed that E(2) significantly stimulates MIF promoter activity. Interestingly, our data further revealed that MIF reciprocally stimulates aromatase protein and mRNA expression via a posttranscriptional mRNA stabilization mechanism, that E(2) itself can upregulate aromatase expression, and that inhibition of endogenous MIF, using MIF specific siRNA, significantly inhibits E(2)-induced aromatase. Thus, the present study revealed the existence of a local positive feedback loop by which estrogen acts directly on ectopic endometrial cells to upregulate the expression of MIF, which, in turn, displays the capability of inducing the expression of aromatase, the key and rate-limiting enzyme for estrogen synthesis. Such interplay may have a considerable impact on the development of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Aromatase Endometriosis Endometriosis Feedback, Physiological Feedback, Physiological Intramolecular Oxidoreductases Macrophage Migration-Inhibitory Factors Adult Aromatase Aromatase Endometriosis Endometriosis Enzyme Induction Enzyme Induction Estradiol Estradiol Estrogen Receptor alpha Estrogen Receptor alpha Estrogen Receptor beta Estrogen Receptor beta

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