Stimulation of macrophage migration inhibitory factor expression in endometrial stromal cells by interleukin 1, beta involving the nuclear transcription factor NFkappaB

W.G. Cao, Cao WG, W-G Cao, Morin M, M. Morin, Metz C, Christine N. Metz, C Metz, Maheux R, R Maheux, Rodolphe Maheux, A Akoum, Ali Akoum, Akoum A
Biology of reproduction · 2005 · vol. 73(3) , pp. 565–570 · doi:10.1095/biolreprod.104.038331 · PMID:15901641 · W2153226227
Lab / animal OA: bronze CC0 ⤵ 45 in-corpus citations
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Interleukin 1 beta stimulates macrophage migration inhibitory factor expression in endometrial stromal cells via the transcription factor NFκB1, a mechanism potentially relevant to endometriosis.

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Abstract

Endometriosis, the ectopic development of endometrial tissue, is, particularly in peritoneal endometriosis, believed to result from tubal reflux of menstrual tissue. The release of cytokines and growth factors by refluxed endometrial cells in response to peritoneal inflammatory stimuli may enhance the capability of endometrial cells to implant and grow into the peritoneal host tissue. Herein we report that interleukin 1 (IL1), a major proinflammatory cytokine that is overproduced by endometriosis women-derived peritoneal macrophages and found in elevated concentrations in the peritoneal fluid of patients with endometriosis, stimulates the synthesis and the secretion of macrophage migration inhibitory factor (MIF) by human endometrial stromal cells. IL1B (0.1-100 ng/ml) exerted dose- and time-dependent effects of MIF protein secretion and mRNA synthesis, as shown by ELISA and reverse transcription-polymerase chain reaction, respectively. IL1B appeared to induce MIF gene transcription via the kappaB nuclear transcription factor (NFkappaB), as shown by electrophoretic mobility shift assay and Western blot analysis of IkappaB phosphorylation. Curcumin (10(-8) M), which is known for inhibiting NFkappaB activation, inhibited IL1B-induced MIF secretion as well as NFkappaB nuclear translocation and DNA binding. Taken together, these findings clearly show that IL1B up-regulates the expression of MIF in endometrial stromal cells in vitro and acts via NFkappaB. This may play an important role in the physiology of the human endometrium and the pathophysiology of endometriosis considering the immunomodulatory properties of MIF as well as its role in cell growth, angiogenesis and tissue remodeling.

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Condition tags

endometriosis

MeSH descriptors

Endometrium Interleukin-1 Macrophage Migration-Inhibitory Factors NF-kappa B Animals Animals Cells, Cultured Cells, Cultured Endometrium Endometrium Endometrium Female Female Gene Expression Regulation Gene Expression Regulation Interleukin-1 Interleukin-1 Macrophage Migration-Inhibitory Factors Macrophage Migration-Inhibitory Factors NF-kappa B

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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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