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Updated: Jul 2, 2026
An Ectopic Chemokine Expression Model for Testing Macrophage Recruitment In Vivo
Published on: September 25, 2019
Involvement of nuclear factor-kappaB in macrophage migration inhibitory factor gene transcription up-regulation
Véronique Veillat1, Catherine Herrmann Lavoie, Christine N Metz
1Unité d'Endocrinologie de la Reproduction, Centre de Recherche, Hôpital Saint-François d'Assise, Centre Hospitalier Universitaire de Québec, Faculté de Médecine, Université Laval, Québec, Canada.
Objective:
To investigate the involvement of the nuclear factor (NF)-kappaB in the interleukin (IL)-1 beta-mediated macrophage migration inhibitory factor (MIF) gene activation.
Design:
Prospective study.
Setting:
Human reproduction research laboratory.
Patient(S):
Nine women with endometriotic lesions.
Intervention(S):
Endometriotic lesions were obtained during laparoscopic surgery.
Main Outcome Measure(S):
The MIF protein secretion was analyzed by ELISA, MIF mRNA expression by quantitative real-time polymerase chain reaction (PCR), NF-kappaB translocation into the nucleus by electrophoresis mobility shift assay, I kappaB phosphorylation and degradation by Western blot, and human MIF promoter activity by transient cell transfection.
Result(S):
This study showed a significant dose-dependent increase of MIF protein secretion and mRNA expression, the NF-kappaB translocation into the nucleus, I kappaB phosphorylation, I kappaB degradation, and human MIF promoter activity in endometriotic stromal cells in response to IL-1 beta. Curcumin (NF-kappaB inhibitor) significantly inhibited all these IL-1 beta-mediated effects. Analysis of the activity of deletion constructs of the human MIF promoter and a computer search localized two putative regulatory elements corresponding to NF-kappaB binding sites at positions -2538/-2528 bp and -1389/-1380 bp.
Conclusion(S):
This study suggests the involvement of the nuclear transcription factor NF-kappaB in MIF gene activation in ectopic endometrial cells in response to IL-1 beta and identifies a possible pathway of endometriosis-associated inflammation and ectopic cell growth.
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