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Submitted on September 26, 2005
Accepted on December 29, 2005
Departments of Clinical Sciences and Biological Sciencesand Physiology, University of Kentucky, Lexington, Kentucky 40506; Pharmacology and Preclinical Development Actelion Pharmaceuticals Ltd, Allschwil, Switzerland; and School of Biotechnology and Biomedical Sciences, Inje University, Kimhae, South Korea
* To whom correspondence should be addressed. E-mail: cko2{at}uky.edu,.
The ovulatory process is activated by a surge of LH (LH), a pituitary gonadotropin, which initiates a cohort of dramatic changes in biochemical, physical, and gene expression in the ovary, leading to follicle rupture and oocyte release. Here we report the identification of endothelin-2 (EDN2) as a last moment-trigger of follicle rupture. In the ovary, EDN2 is exclusively and transiently expressed in the granulosa cells immediately before ovulation. Administration of EDN2 to the ovarian tissue induced rapid contraction, while addition of tezosentan, an endothelin receptor antagonist, diminishes the EDN2 effect. In vivo, treatment of tezosentan before ovulation substantially decreases gonadotropin-induced superovulation. As a target tissue of EDN2 action, we identified a layer of smooth muscle cells in the follicular wall of each follicle. Taken together, our data indicate that EDN2 induces follicular rupture by constricting periovulatory follicles.
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