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Updated: Jul 10, 2026
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
[Temporal and spatial expression of estrogen activity-related molecules in eutopic endometrium of adenomyosis]
Zhi-rong Guo1, Ju Zhang, Jing-he Lang
1State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, China & Bioactive Materials Key Laboratory of Ministry of Education, Life Science College, Nankai University, Tianjing 200000, China.
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.
