[Temporal and spatial expression of estrogen activity-related molecules in eutopic endometrium of adenomyosis].

Abstract

OBJECTIVE:

The aim of this study was to demonstrate the temporal and spatial expression of estrogen receptor (ER), 17beta-hydroxysteroid dehydrogenase (17beta-HSD) in uterine endometria and the endometrial-myometrial interface (EMI) of adenomyosis and the effects of estrogen activity-related molecules on the occurrence of adenomyosis.

METHODS:

Thirty-three cases of normal endometria (and myometrial) and eighteen cases of endometria (and myometrial) with adenomyosis were collected. Immunohistochemical assay was performed to locate the ERalpha, ERbeta, 17beta-HSDI and 17beta-HSDII in endometria and EMI.

RESULTS:

The ERalpha positive cell number in glandular epithelial cells at the early proliferative phase increased evidently in adenomyosis (90%), while it was 60% in normal endometria. We found ERalpha signal in cytoplasm in glandular epithelial cells of adenomyosis endometria as well as in nucleus. Compared with normal endometrium (early proliferative phase: +; late proliferative phase: ++; late secretory phase: +), eutopic endometrium with adenomyosis exhibited a higher level of 17beta-HSDI (early proliferative phase: ++; late proliferative phase: +++; late secretory phase: ++). The intensity of 17beta-HSDIIin glandular epithelial cells of eutopic endometrium with adenomyosis (early proliferative phase: +++; secretory phase: ++++) was also higher than that of normal endometrium (early proliferative phase: - approximately ++; secretory phase: +++). Higher intensities of ERalpha, ERbeta and 17beta-HSDIand lower intensities of 17beta-HSDII were observed in EMI than in the eutopic endometrium of adenomyosis.

CONCLUSIONS:

The elevation of ERalpha positive cell number, 17beta-HSDI level as well as the insufficient compensation of 17beta-HSDII in eutopic endometrium with adenomyosis and the change in expression pattern of ERalpha, ERbeta, 17beta-HSDI and 17beta-HSDII in EMI lead to the local enhancement of estrogen effect, which would promote cell proliferation.

• Authors: Zhi-rong Guo, Ju Zhang, Jing-he Lang, Jin-hua Leng, Yun-shang Piao, Yan-ling Wang
• Journal: Zhonghua fu chan ke za zhi (Zhonghua Fu Chan Ke Za Zhi) Vol. 39 Issue 4 Pg. 246-9 (Apr 2004) ISSN: 0529-567X [Print] China
• PMID: 15130351 (Publication Type: Comparative Study, English Abstract, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Estrogen Receptor alpha
• Estrogen Receptor beta
• Receptors, Estrogen
• 17-Hydroxysteroid Dehydrogenases
• 3 (or 17)-beta-hydroxysteroid dehydrogenase

Topics

• 17-Hydroxysteroid Dehydrogenases (analysis)
• Adult
• Choristoma (metabolism, pathology)
• Endometriosis (metabolism, pathology)
• Estrogen Receptor alpha
• Estrogen Receptor beta
• Female
• Humans
• Immunohistochemistry
• Menstrual Cycle (metabolism)
• Middle Aged
• Receptors, Estrogen (analysis)