Involvement of nuclear factor-?B in macrophage migration inhibitory factor gene transcription up-regulation induced by interleukin-1ß in ectopic endometrial cells  

Oleh:

Veillat, Véronique ; Lavoie, Catherine Herrmann ; Metz, Christine N. ; Roger, Thierry

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 91 no. 5 Sup (May 2009), page 2148-2156.
Topik: Ectopic endometrial cells; IL-1ß; MIF; NF-?B

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2009.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Objective : To investigate the involvement of the nuclear factor (NF)-?B in the interleukin (IL)-1ß-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-?B translocation into the nucleus by electrophoresis mobility shift assay, I?B 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-?B translocation into the nucleus, I?B phosphorylation, I?B degradation, and human MIF promoter activity in endometriotic stromal cells in response to IL-1ß. Curcumin (NF-?B inhibitor) significantly inhibited all these IL-1ß-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-?B binding sites at positions -2538/-2528 bp and -1389/-1380 bp. Conclusion(s) : This study suggests the involvement of the nuclear transcription factor NF-?B in MIF gene activation in ectopic endometrial cells in response to IL-1ß and identifies a possible pathway of endometriosis-associated inflammation and ectopic cell growth.

Opini Anda

Klik untuk menuliskan opini Anda tentang koleksi ini!

Kembali