Disturbed estrogen and progesterone action in ovarian endometriosis

• Published in: Molecular and cellular endocrinology 2009-03, Vol.301 (1), p.59-64
• Main Authors: Šmuc, Tina, Hevir, Neli, Ribič-Pucelj, Martina, Husen, Bettina, Thole, Hubert, Rižner, Tea Lanišnik
• Format: Article
• Language: English
• Subjects: 17-Hydroxysteroid Dehydrogenases - metabolism; 17β-Hydroxysteroid dehydrogenases; 20-Hydroxysteroid Dehydrogenases - metabolism; 3-Hydroxysteroid Dehydrogenases - metabolism; Aberration; Adult; AKR1C1; AKR1C3; Aldo-Keto Reductase Family 1 Member C3; Aromatase - metabolism; Endometriosis; Endometriosis - enzymology; Endometriosis - metabolism; Estrogen and progesterone receptors; Estrogen Receptor alpha - metabolism; Estrogen Receptor beta - metabolism; Estrogen- and progesterone-metabolizing enzymes; Estrogens - metabolism; Female; Humans; Hydroxyprostaglandin Dehydrogenases - metabolism; Immunohistochemistry; Middle Aged; Ovary - enzymology; Ovary - metabolism; Ovary - pathology; Progesterone - metabolism; Receptors, Progesterone - metabolism; Sulfotransferases
• ISSN: 0303-7207; 1872-8057; 0303-7207
• DOI: 10.1016/j.mce.2008.07.020

Endometriosis is a very common disease in pre-menopausal women, where defective metabolism of steroid hormones plays an important role in its development and promotion. In the present study, we have examined the expression of 11 estrogen and progesterone metabolizing enzymes and their corresponding receptors in samples of ovarian endometriomas and control endometrium. Expression analysis revealed significant up-regulation of enzymes involved in estradiol formation (aromatase, sulfatase and all reductive 17β-hydroxysteroid dehydrogenases) and in progesterone inactivation (AKR1C1 and AKR1C3). Among the estrogen and progesterone receptors, ERα was down-regulated, ERβ was up-regulated, and there was no significant difference in expression of progesterone receptors A and B (PRAB). Our data indicate that several enzymes of estrogen and progesterone metabolism are aberrantly expressed in endometriosis, which can lead to increased local levels of mitogenic estradiol and decreased levels of protective progesterone. Changes in estrogen receptor expression suggest that estradiol may also act via non-estrogen receptor-mediated pathways, while expression of progesterone receptors still needs further investigation.