The Cellular Inhibitor of Apoptosis Protein-2 is a Possible Target of Novel Treatment for Endometriosis
Version of Record online: 2 JAN 2014
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
American Journal of Reproductive Immunology
Volume 71, Issue 3, pages 278–285, March 2014
How to Cite
The cellular inhibitor of apoptosis (cIAP) protein-2 is a possible target of novel treatment for endometriosis. Am J Reprod Immunol 2014; 71: 278–285, , , , , , , , .
- Issue online: 7 FEB 2014
- Version of Record online: 2 JAN 2014
- Manuscript Accepted: 2 DEC 2013
- Manuscript Received: 24 JUL 2013
- KAKENHI. Grant Number: 21592098
- Cellular inhibitor of apoptosis protein -2;
- Nuclear factor-κB pathway;
- tumor necrosis factor α
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.
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.
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.