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Low expression of COX-2, reduced cumulus expansion, and impaired ovulation in SULT1E1-deficient mice
Year:
2007
Source of publication :
FASEB Journal
Authors :
Gershon, Eran
;
.
Volume :
21
Co-Authors:
Gershon, E., Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel
Hourvitz, A., Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel, In Vitro Fertilization (IVF) Unit, Department of Obstetrics and Gynecology, Chaim Sheba Medical Center, Tel Hashomer, Ramat-Gan, Israel
Reikhav, S., Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel
Maman, E., In Vitro Fertilization (IVF) Unit, Department of Obstetrics and Gynecology, Chaim Sheba Medical Center, Tel Hashomer, Ramat-Gan, Israel
Dekel, N., Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel, Department of Biological Regulation, Weizmann Institute of Science, P.O.B. 26, Rehovot 76100, Israel
Facilitators :
From page:
1893
To page:
1901
(
Total pages:
9
)
Abstract:
The SULT1E1-encoded estrogen sulfotransferase (EST) catalyzes sulfation of estrogen, resulting in its inactivation. Reduced fertility observed in SULT1E1 knockout (KO) female mice has previously been attributed to the deleterious effect of chronic exposure to high levels of circulating estrogen on placental function. We herein suggest that, in addition to placental dysfunction, this phenotype demonstrates that an excess of estrogen impairs ovulation. The role of SULT1E1 in ovulation is suggested by the substantially low ovulatory response in hCG-treated SULT1E1 KO mice; a similar effect was observed when 17β-estradiol was administered to wild-type (WT) females. The normal rate of ovulation in SULT1E1 KO females may be restored by PGE2. Along this line, ovaries of human Chorionic Gonadotropin (hCG)-treated SULT1E1 KO mice expressed low levels of cyclooxygenase-2 (COX-2) and its downstream TSG6; moreover, their ovaries contained a reduced number of expanded cumuli. Our results demonstrate, for the first time, that estrogen inactivation may allow the expression of COX-2 and subsequent cumulus expansion, enabling normal ovulation. Our findings may be applied to novel treatments of human ovulatory failure. © FASEB.
Note:
Related Files :
animal experiment
Animals
animal tissue
Female
Infertility
mice
phenotype
Sulfotransferases
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Related Content
More details
DOI :
10.1096/fj.06-7688com
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
28589
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:40
Scientific Publication
Low expression of COX-2, reduced cumulus expansion, and impaired ovulation in SULT1E1-deficient mice
21
Gershon, E., Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel
Hourvitz, A., Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel, In Vitro Fertilization (IVF) Unit, Department of Obstetrics and Gynecology, Chaim Sheba Medical Center, Tel Hashomer, Ramat-Gan, Israel
Reikhav, S., Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel
Maman, E., In Vitro Fertilization (IVF) Unit, Department of Obstetrics and Gynecology, Chaim Sheba Medical Center, Tel Hashomer, Ramat-Gan, Israel
Dekel, N., Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel, Department of Biological Regulation, Weizmann Institute of Science, P.O.B. 26, Rehovot 76100, Israel
Low expression of COX-2, reduced cumulus expansion, and impaired ovulation in SULT1E1-deficient mice
The SULT1E1-encoded estrogen sulfotransferase (EST) catalyzes sulfation of estrogen, resulting in its inactivation. Reduced fertility observed in SULT1E1 knockout (KO) female mice has previously been attributed to the deleterious effect of chronic exposure to high levels of circulating estrogen on placental function. We herein suggest that, in addition to placental dysfunction, this phenotype demonstrates that an excess of estrogen impairs ovulation. The role of SULT1E1 in ovulation is suggested by the substantially low ovulatory response in hCG-treated SULT1E1 KO mice; a similar effect was observed when 17β-estradiol was administered to wild-type (WT) females. The normal rate of ovulation in SULT1E1 KO females may be restored by PGE2. Along this line, ovaries of human Chorionic Gonadotropin (hCG)-treated SULT1E1 KO mice expressed low levels of cyclooxygenase-2 (COX-2) and its downstream TSG6; moreover, their ovaries contained a reduced number of expanded cumuli. Our results demonstrate, for the first time, that estrogen inactivation may allow the expression of COX-2 and subsequent cumulus expansion, enabling normal ovulation. Our findings may be applied to novel treatments of human ovulatory failure. © FASEB.
Scientific Publication
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