P450Arom induction in isolated control endometrial cells by peritoneal fluid from women with endometriosis
Author
dc.contributor.author
Castro, Jazmín
Author
dc.contributor.author
Torres, Marisa
Author
dc.contributor.author
Sovino, Hugo
Author
dc.contributor.author
Fuentes, Ariel
Author
dc.contributor.author
Boric, María Angélica
Author
dc.contributor.author
Johnson, M. Cecilia
Admission date
dc.date.accessioned
2019-03-11T13:00:48Z
Available date
dc.date.available
2019-03-11T13:00:48Z
Publication date
dc.date.issued
2010
Cita de ítem
dc.identifier.citation
Fertility and Sterility, Volumen 94, Issue 7, 2010, Pages 2521-2527
Identifier
dc.identifier.issn
00150282
Identifier
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10.1016/j.fertnstert.2010.03.036
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/165147
Abstract
dc.description.abstract
Objective: To study the effect of peritoneal fluid from women with (PF-E) and without (PF-C) endometriosis on
P450Arom expression in endometrial cells.
Design: Experimental study.
Setting: University research unit.
Patient(s): Forty women of reproductive age with (n ¼ 22) or without (control; n ¼ 18) endometriosis.
Intervention(s): Peritoneal fluid and eutopic endometrial samples were obtained during surgery from women with
(n ¼ 13 and 9, respectively) and without (n ¼ 4 and 14, respectively) endometriosis.
Main Outcome Measure(s): Expression study for P450Arom, steroid factor 1 (SF-1), chicken ovalbumin upstream
transcription factor I (COUP-TFI), and COUP-TFII messenger RNA (reverse transcriptase–polymerase chain
reacion) and/or protein (immunoblot) in isolated endometrial epithelial cells transfected or not with expression
vector containing SF-1, COUP-TFI, or COUP-TFII complementary DNAs.
Result(s): Basal messenger RNA and/or protein expression of P450Arom and SF-1 were augmented in endometriosis,
and that of COUP-TF was diminished. In control cells, (Bu)2cAMP and PF-E increased P450Arom and SF-1
expression (but not COUP-TF expression) in a dose-dependent way, an effect not observed with PF-C, adsorbed
PF-E, or 10 5 M indomethacin. Transfected cells confirmed these results. Any treatments modified the studied
molecules in endometriosis cells.
Conclusion(s): These data indicate that molecules contained in PF-E favor an estrogenic microenvironment,
suggesting a role in the etiopathogenesis of endometriosis enabling the survival, maintenance, and growth of
endometrial implants in the ectopic locations.