Effects of hormones on uPA, PAI-1 and suPAR from cultured endometrial and ovarian endometriotic stromal cells.
OBJECTIVE
To investigate whether endometriotic stromal cells release the urokinase plasminogen activator, soluble urokinase plasminogen activator receptor and plasminogen activator inhibitor-1. If so, to establish if there are any differences between endometrial stromal cells from women with and without endometriosis, and whether the release is hormonally regulated.


METHODS
Biopsies were obtained from endometriotic tissue and from endometrium from women with and without endometriosis. Stromal cells were isolated, incubated and treated with estradiol-17beta, progesterone or raloxifen. Incubation media collected at 0, 24, 48 and 72 h were analyzed by enzyme-linked immunosorbent assay.


RESULTS
All these types of stromal cells released the urokinase plasminogen activator, soluble urokinase plasminogen activator receptor and urokinase plasminogen inhibitor-1. There was a significantly higher release of urokinase plasminogen inhibitor-1 and lower release of urokinase plasminogen activator and soluble urokinase plasminogen activator receptor in endometriotic cells. The release of urokinase plasminogen activator from endometrial stromal cells decreased during the study period both in control cultures and in cultures treated with progesterone or estradiol-17beta, but not in cultures treated with raloxifen nor in endometriotic cultures. The given hormones did not influence the release of the soluble urokinase plasminogen activator receptor. Progesterone significantly increased the urokinase plasminogen inhibitor-1 release in endometrial cells from both patient categories, and raloxifen significantly reduced the urokinase plasminogen inhibitor-1 release from stromal cells from both tissue categories from endometriotic patients. Estradiol-17beta had no effect.


CONCLUSIONS
This study shows that stromal cells from endometrium and endometriotic tissues release the urokinase plasminogen activator, soluble urokinase plasminogen activator receptor and urokinase plasminogen inhibitor-1. The release is partly hormonally regulated, but differently in endometriotic than in endometrial cells.
Guan
Yong-Mei
YM
Department of Clinical Sciences, Unit for Obstetrics and Gynecology, Huddinge University Hospital, Stockholm, Sweden.
Carlberg
Magdalena
M
Bruse
Christine
C
Carlström
Kjell
K
Bergqvist
Agneta
A
D000328:Adult; D016022:Case-Control Studies; D002460:Cell Line / Q000187:drug effects / Q000378:metabolism; D004715:Endometriosis / Q000378:metabolism*; D004717:Endometrium / Q000166:cytology; D004797:Enzyme-Linked Immunosorbent Assay; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D006728:Hormones / Q000494:pharmacology*; D006801:Humans; D008875:Middle Aged; D010053:Ovary / Q000166:cytology; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism*; D011374:Progesterone / Q000494:pharmacology; D020849:Raloxifene Hydrochloride / Q000494:pharmacology; D011956:Receptors, Cell Surface / Q000187:drug effects* / Q000378:metabolism; D055293:Receptors, Urokinase Plasminogen Activator; D017154:Stromal Cells / Q000187:drug effects* / Q000378:metabolism; D014568:Urokinase-Type Plasminogen Activator / Q000187:drug effects* / Q000378:metabolism
D006728:Hormones; C524898:PLAUR protein, human; D017395:Plasminogen Activator Inhibitor 1; D011956:Receptors, Cell Surface; D055293:Receptors, Urokinase Plasminogen Activator; D020849:Raloxifene Hydrochloride; D011374:Progesterone; D004958:Estradiol; D014568:Urokinase-Type Plasminogen Activator