Results
| PMID | 18710704 |
| Gene Name | MIF |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 9 |
| Population details | 9 women with endometriotic lesions |
| Sex | Female |
| Associated genes | MIF |
| Other associated phenotypes |
Ectopic endometriosis |
|
Fertil Steril. 2009 May;91(5 Suppl):2148-56. doi: Veillat, Veronique| Lavoie, Catherine Herrmann| Metz, Christine N| Roger, Thierry| Labelle, Yves| Akoum, Ali Unite d'Endocrinologie de la Reproduction, Centre de Recherche, Hopital Saint-Francois d'Assise, Centre Hospitalier Universitaire de Quebec, Faculte de Medecine, Universite Laval, Quebec, 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. Mesh Terms: Cell Culture Techniques| Endometriosis/*genetics/pathology| Female| Humans| Interleukin-1beta/*pharmacology| Macrophage Migration-Inhibitory Factors/*genetics| NF-kappa B/*physiology| Pregnancy| Pregnancy, Ectopic/genetics| RNA, Messenger/genetic |
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