1. The cellular inhibitor of apoptosis protein-2 is a possible target of novel treatment for endometriosis.
- Author
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Taniguchi F, Higaki H, Izawa M, Azuma Y, Hirakawa E, Deura I, Iwabe T, Hata K, and Harada T
- Subjects
- Cell Proliferation drug effects, Cells, Cultured, Endometriosis drug therapy, Female, Gene Expression Regulation drug effects, Humans, I-kappa B Proteins metabolism, Inhibitor of Apoptosis Proteins antagonists & inhibitors, Inhibitor of Apoptosis Proteins genetics, Interleukin-8 metabolism, Molecular Targeted Therapy, NF-kappa B antagonists & inhibitors, Oligopeptides pharmacology, Phosphorylation drug effects, Signal Transduction drug effects, Stromal Cells drug effects, Tosylphenylalanyl Chloromethyl Ketone pharmacology, Tumor Necrosis Factor-alpha immunology, Endometriosis immunology, Endometrium pathology, Inhibitor of Apoptosis Proteins metabolism, Stromal Cells physiology
- Abstract
Problem: How is the tumor necrosis factor (TNF) α-induced inhibitor of apoptosis (IAP) protein expression in endometriotic stromal cells (ESCs) involved in cell viability and signaling pathways?, Method of Study: Endometriotic stromal cells were isolated from ovarian chocolate cysts in 20 patients who underwent laparoscopic surgery. IAP protein expression and IκB phosphorylation were evaluated by Western blot analysis. Interleukin (IL)-8 protein expression and cell proliferation were assessed by ELISA., Results: Cellular IAP (cIAP)-2 protein expression in endometriotic tissue was higher than that of endometrium. TNFα markedly enhanced cIAP-2 protein expression in ESCs. Pretreatment with a nuclear factor (NF)-κB inhibitor attenuated TNFα-induced cIAP-2 expression. An antagonist of IAPs abrogated TNFα-induced cIAP-2 protein expression and showed a decrease in TNFα-induced IL-8 protein expression and BrdU incorporation in ESCs., Conclusions: TNFα and its downstream NFκB pathway have proven to be critical regulators of highly expressed cIAP-2 in ESCs. cIAP-2 may be a novel therapeutic target for endometriosis., (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
- Published
- 2014
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