title: The cellular inhibitor of apoptosis protein-2 is a possible target of novel treatment for endometriosis.
abstract: OBJECTIVE
  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?
  
  
  METHODS
  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.
authors.affiliation: Department of Obstetrics and Gynecology, Tottori University Faculty of Medicine, Yonago, Japan.
authors.forename: Fuminori
authors.initials: F
authors.lastname: Taniguchi
authors.forename: Hiroko
authors.initials: H
authors.lastname: Higaki
authors.forename: Masao
authors.initials: M
authors.lastname: Izawa
authors.forename: Yukihiro
authors.initials: Y
authors.lastname: Azuma
authors.forename: Eriko
authors.initials: E
authors.lastname: Hirakawa
authors.forename: Imari
authors.initials: I
authors.lastname: Deura
authors.forename: Tomio
authors.initials: T
authors.lastname: Iwabe
authors.forename: Kohkichi
authors.initials: K
authors.lastname: Hata
authors.forename: Tasuku
authors.initials: T
authors.lastname: Harada
mesh_terms: D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D004715:Endometriosis / Q000188:drug therapy / Q000276:immunology*; D004717:Endometrium / Q000473:pathology*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D051034:Inhibitor of Apoptosis Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D016209:Interleukin-8 / Q000378:metabolism; D058990:Molecular Targeted Therapy; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D009842:Oligopeptides / Q000494:pharmacology; D010766:Phosphorylation / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects; D017154:Stromal Cells / Q000187:drug effects / Q000502:physiology*; D014108:Tosylphenylalanyl Chloromethyl Ketone / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: C582180:BV6 peptide; C083487:I kappa B beta protein; D020672:I-kappa B Proteins; D051034:Inhibitor of Apoptosis Proteins; D016209:Interleukin-8; D016328:NF-kappa B; D009842:Oligopeptides; D014409:Tumor Necrosis Factor-alpha; D014108:Tosylphenylalanyl Chloromethyl Ketone
keywords: Cellular inhibitor of apoptosis protein -2; Nuclear factor-κB pathway; tumor necrosis factor α