Iron overload–modulated nuclear factor kappa-B activation in human endometrial stromal cells as a mechanism postulated in endometriosis pathogenesis  

Oleh:

Alvarado-Diaz, Carlos Patricio ; Nunez, Marco Tulio ; Devoto, Luigi ; Gonzalez-Ramos, Reinaldo

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 103 no. 02 (Feb. 2015), page 439-447.
Topik: Endometriosis; endometrium; iron overload; NF-?B; ICAM-1

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K Non-tandon: tidak ada Tandon: 1

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Isi artikel

Objective To evaluate the effect of iron overload on nuclear factor kappa-B (NF-?B) activation in human endometrial stromal cells (ESCs). Design Experimental study. Setting University hospital research laboratory. Patient(s) Ten healthy women. Intervention(s) Isolated ESCs from endometrial biopsies were incubated with 50 µM FeSO4 or vehicle. The NF-?B inhibitor [5-(p-fluorophenyl)-2-ureido] thiophene-3-carboxamide (TPCA-1), which inhibits IKKß, the kinase of I?Ba (inhibitory protein of NF-?B), was used to prevent iron overload–stimulated NF-?B changes in ESCs. Main Outcome Measure(s) NF-?B activation was assessed by p65:DNA-binding activity immunodetection assay. I?Ba, p65, and intercellular adhesion molecule (ICAM)-1 proteins expression was evaluated by Western blots. ESC soluble ICAM (sICAM)-1 secretion was measured by ELISA using conditioned medium. Result(s) Iron overload increased p65:DNA-binding activity and decreased I?Ba and p65 cytoplasmic expression in ESCs after 30 minutes of incubation as compared with the basal condition. ESC ICAM-1 expression and sICAM-1 secretion were higher after 24 hours of iron overload treatment than in the absence of treatment. TPCA-1 prevented the iron overload–induced increase of p65:DNA binding and I?Ba degradation. Conclusion(s) Iron overload activates IKKß in ESCs, stimulating the NF-?B pathway and increasing ICAM-1 expression and sICAM-1 secretion. These results suggest that iron overload induces a proendometriotic phenotype on healthy ESCs, which could participate in endometriosis pathogenesis and development.

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