title: Stromal cells from endometriotic lesions and endometrium from women with endometriosis have reduced decidualization capacity.
abstract: OBJECTIVE
  To evaluate the phenotype, proliferative, and differentiation capacities in vitro of stromal cells derived from peritoneal, ovarian, and deeply infiltrating endometriosis.
  
  
  METHODS
  Experimental study using phase contrast microscopy, immunocytochemistry, and functional bioassays.
  
  
  METHODS
  University-based laboratory.
  
  
  METHODS
  Women with and without endometriosis undergoing surgery for benign indications.
  
  
  METHODS
  None.
  
  
  METHODS
  The stability in vitro of stromal cells derived from peritoneal (n = 18), ovarian (n = 29), and deeply infiltrating (n = 14) endometriotic lesions, as well as endometrium from women with (n = 5) and without endometriosis (n = 5) was evaluated by detection of endometrial markers. The proliferative and differentiation capacity of the cells was assessed by the use of cell doubling estimation and in vitro decidualization assays.
  
  
  RESULTS
  The expression of the progesterone receptor and CD10 in stromal cells derived from the three types of endometriotic lesions is retained in culture up to passage 10. The doubling time of stromal cells from deeply infiltrating lesions is lower than that of endometrial stromal cells. Levels of prolactin and insulin-like growth factor binding protein-1 (IGFBP-1) are reduced in supernatants from stromal cells derived from the three types of lesions and from the endometrium of women with endometriosis.
  
  
  CONCLUSIONS
  The peritoneal, ovarian, and deeply infiltrating endometriotic stromal cell lines we describe retain in vivo tissue markers. Loss of differentiation capacity of the endometriotic cell lines and endometrial cells from women with endometriosis may influence the capacity for proliferation and survival of these cells in the ectopic environment.
authors.affiliation: Nuffield Department of Obstetrics and Gynaecology, The Women's Centre, John Radcliffe Hospital, Oxford, United Kingdom.
authors.forename: Petra A B
authors.initials: PA
authors.lastname: Klemmt
authors.forename: Janet G
authors.initials: JG
authors.lastname: Carver
authors.forename: Stephen H
authors.initials: SH
authors.lastname: Kennedy
authors.forename: Philippe R
authors.initials: PR
authors.lastname: Koninckx
authors.forename: Helen J
authors.initials: HJ
authors.lastname: Mardon
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D002454:Cell Differentiation; D049109:Cell Proliferation; D002478:Cells, Cultured; D003656:Decidua / Q000503:physiopathology*; D004715:Endometriosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D004717:Endometrium / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000378:metabolism; D008875:Middle Aged; D015260:Neprilysin / Q000378:metabolism; D010049:Ovarian Diseases / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D010532:Peritoneal Diseases / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D010641:Phenotype; D011388:Prolactin / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D017154:Stromal Cells / Q000378:metabolism / Q000473:pathology; D013997:Time Factors
chemical_list: D015415:Biomarkers; D018970:Insulin-Like Growth Factor Binding Protein 1; D011980:Receptors, Progesterone; D011388:Prolactin; D015260:Neprilysin