Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (29)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Fujimoto, J.
Right arrow Articles by Tamaya, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fujimoto, J.
Right arrow Articles by Tamaya, T.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Molecular Human Reproduction, Vol. 5, No. 8, 742-747, August 1999
© 1999 European Society of Human Reproduction and Embryology

Expression of oestrogen receptor-{alpha} and -ß in ovarian endometriomata

J. Fujimoto1,2, R. Hirose1, H. Sakaguchi1 and T. Tamaya1

1 Department of Obstetrics and Gynecology, Gifu University School of Medicine, 40 Tsukasa-machi, Gifu City 500-8705, Japan

The contribution of oestrogen receptor (ER) isoforms, ER-{alpha} and ER-ß, in oestrogen-dependent development and growth of ovarian endometriomata, is unknown. Therefore, we examined the expression of ER-{alpha} and ER-ß in ovarian endometriomata and normal uterine endometrium. ER-{alpha} and ER-ß were shown to be dominantly expressed in the nuclei of the epithelial lining cells of ovarian endometrioma and of the glandular cells of normal uterine endometrium. ER-ß was expressed at a much lower level than ER-{alpha} in the glandular cells of normal uterine endometrium, while ER-ß was expressed at a slightly lower level than ER-{alpha} in the epithelial lining cells of ovarian endometrioma. In normal uterine endometrium, ER-ß mRNA was expressed at a much lower level than ER-{alpha} mRNA, and the expression pattern of ER-ß mRNA during the menstrual cycle was similar to that of ER-{alpha} mRNA. On the other hand, ER-ß mRNA expression was significantly higher and over a much greater range in ovarian endometriomata (P < 0.05) than in normal uterine endometrium during the menstrual cycle, while ER-{alpha} mRNA expression was relatively lower and more random. Therefore, in ovarian endometriomata, oestrogen action via ER-{alpha} cascades seems to be partially damaged, as the expression of ER-{alpha} mRNA does not respond to endocrinological alterations during the menstrual cycle, while the relative over-expression of ER-ß might be related to a unique oestrogen-dependent growth and spreading of ovarian endometriomata.

ER-{alpha}/ER-ß/ovarian endometrioma

2 To whom correspondence should be addressed


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Biol. Reprod.Home page
Q. Xue, Z. Lin, Y.-H. Cheng, C.-C. Huang, E. Marsh, P. Yin, M. P Milad, E. Confino, S. Reierstad, J. Innes, et al.
Promoter Methylation Regulates Estrogen Receptor 2 in Human Endometrium and Endometriosis
Biol Reprod, October 1, 2007; 77(4): 681 - 687.
[Abstract] [Full Text] [PDF]


Home page
Biol. Reprod.Home page
W. X. Liao, R. R. Magness, and D.-b. Chen
Expression of Estrogen Receptors-{alpha} and -{beta} in the Pregnant Ovine Uterine Artery Endothelial Cells In Vivo and In Vitro
Biol Reprod, March 1, 2005; 72(3): 530 - 537.
[Abstract] [Full Text] [PDF]


Home page
Ann OncolHome page
J. Fujimoto, I. Aoki, H. Toyoki, S. Khatun, and T. Tamaya
Clinical implications of expression of ETS-1 related to angiogenesis in uterine cervical cancers
Ann. Onc., October 1, 2002; 13(10): 1598 - 1604.
[Abstract] [Full Text] [PDF]


Home page
Ann OncolHome page
J. Fujimoto, I. Aoki, H. Toyoki, S. Khatun, and T. Tamaya
Clinical implications of expression of ETS-1 related to angiogenesis in uterine endometrial cancers
Ann. Onc., October 1, 2002; 13(10): 1605 - 1611.
[Abstract] [Full Text] [PDF]


Home page
Mol Hum ReprodHome page
H. Okada, T. Nakajima, T. Yoshimura, K. Yasuda, and H. Kanzaki
The inhibitory effect of dienogest, a synthetic steroid, on the growth of human endometrial stromal cells in vitro
Mol. Hum. Reprod., April 1, 2001; 7(4): 341 - 347.
[Abstract] [Full Text] [PDF]


Home page
J. Clin. Endocrinol. Metab.Home page
H. O. D. Critchley, R. M. Brenner, T. A. Henderson, K. Williams, N. R. Nayak, O. D. Slayden, M. R. Millar, and P. T. K. Saunders
Estrogen Receptor {beta}, But Not Estrogen Receptor {{alpha}}, Is Present in the Vascular Endothelium of the Human and Nonhuman Primate Endometrium
J. Clin. Endocrinol. Metab., March 1, 2001; 86(3): 1370 - 1378.
[Abstract] [Full Text]


Home page
J. Clin. Endocrinol. Metab.Home page
G. LECCE, G. MEDURI, M. ANCELIN, C. BERGERON, and M. PERROT-APPLANAT
Presence of Estrogen Receptor {beta} in the Human Endometrium through the Cycle: Expression in Glandular, Stromal, and Vascular Cells
J. Clin. Endocrinol. Metab., March 1, 2001; 86(3): 1379 - 1386.
[Abstract] [Full Text]


Home page
Hum ReprodHome page
J. Kitawaki, H. Obayashi, H. Ishihara, H. Koshiba, I. Kusuki, N. Kado, K. Tsukamoto, G. Hasegawa, N. Nakamura, and H. Honjo
Oestrogen receptor-alpha gene polymorphism is associated with endometriosis, adenomyosis and leiomyomata
Hum. Reprod., January 1, 2001; 16(1): 51 - 55.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
Z. Weihua, S. Saji, S. Makinen, G. Cheng, E. V. Jensen, M. Warner, and J.-A. Gustafsson
Estrogen receptor (ER) beta , a modulator of ERalpha in the uterus
PNAS, May 23, 2000; 97(11): 5936 - 5941.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.