Stromal cells from endometriotic lesions and endometrium from women with endometriosis have reduced decidualization capacity.
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.
Klemmt
Petra A B
PA
Nuffield Department of Obstetrics and Gynaecology, The Women's Centre, John Radcliffe Hospital, Oxford, United Kingdom.
Carver
Janet G
JG
Kennedy
Stephen H
SH
Koninckx
Philippe R
PR
Mardon
Helen J
HJ
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
D015415:Biomarkers; D018970:Insulin-Like Growth Factor Binding Protein 1; D011980:Receptors, Progesterone; D011388:Prolactin; D015260:Neprilysin