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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 125-134 |
| Number of pages | 10 |
| Journal | Seminars in reproductive medicine |
| Volume | 21 |
| Issue number | 2 |
| DOIs | |
| State | Published - May 2003 |
Keywords
- 17β-hydroxysteroid dehydrogenase type 2
- Aromatase
- Aromatase inhibitor
- Endometriosis
- Endometrium
- Estradiol
- Estrogen
- Estrogen biosynthesis
- Estrogen metabolism
- Estrone
- Progesterone
- Progesterone receptor
- Steroidogenesis
ASJC Scopus subject areas
- Physiology (medical)
- Endocrinology
- Obstetrics and Gynecology
- Endocrinology, Diabetes and Metabolism
- Reproductive Medicine
