ABSTRACT
Estrogen is an extremely potent mitogen for endometrium and endometriosis. Progesterone,
on the other hand, inhibits the mitogenic action of estrogen on endometrium and enhances
differentiation. These antiproliferative and differentiative effects of progesterone
are less pronounced on endometriosis tissue compared with endometrium. Thus, endometriosis
is, at least in part, resistant to progesterone action. The product of a single gene
named aromatase synthesizes estrogen. The potent estrogen estradiol is metabolized
and thus inactivated by an enzyme termed 17β-hydroxysteroid dehydrogenase (HSD) type
2 that is normally induced by progesterone in endometrium. Progesterone action is
mediated by its receptor subtypes progesterone receptor (PR)-A and PR-B. We found
a number of abnormalities in the expression of aromatase, 17β-HSD type 2, and the
PR-B/PR-A ratio in endometriosis tissue. These abnormalities and their functional
consequences are discussed in this review article.
KEYWORDS
Endometriosis - aromatase - aromatase inhibitor - endometrium - estrogen - estrogen
biosynthesis - estrogen metabolism - 17β-hydroxysteroid dehydrogenase type 2 - steroidogenesis
- progesterone - estrone - estradiol - progesterone receptor