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Endothelin-2 in Ovarian Follicle Rupture

Departments of Clinical Sciences and Biological Sciences (C.K., M.C.Gi., L.A.-A., Y.H.) and Physiology (W.S., M.C.Go.), University of Kentucky, Lexington, Kentucky 40506; Pharmacology and Preclinical Development Actelion Pharmaceuticals Ltd. (M.I.), Allschwil CH-4123, Switzerland; and School of Biotechnology and Biomedical Sciences (Y.K.), Inje University, Kimhae 621-749, South Korea

Address all correspondence and requests for reprints to: Dr. Chemyong Ko, Department of Clinical Sciences, University of Kentucky, Lexington, Kentucky 40536. E-mail: cko2{at}uky.edu.

The ovulatory process is activated by a surge of 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, whereas 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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