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Ovulation in Plasminogen-Deficient Mice¹

Department of Medical Biosciences, Medical Biochemistry, Umeå University (A.N., G.L., A.-C.H., P.H., T.N.), S-901 87 Umeå, Sweden; the Department of Chemistry and Biochemistry, University of Notre Dame (V.A.P.), Notre Dame, Indiana 46556-5670; and the Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Instituut voor Biotechnologie (P.C.), B-3000 Leuven, Belgium

Address all correspondence and requests for reprints to: Dr. Tor Ny, Department of Medical Biosciences, Medical Biochemistry, Umeå University, S-901 87 Umeå, Sweden. E-mail: tor.ny{at}medchem.umu.se

Many different studies suggest that plasmin generated from plasminogen plays a crucial role in the degradation of the follicular wall at the time of ovulation. We have assessed the physiological relevance of plasmin on ovulation by studying plasminogen-deficient mice. Ovulation efficiency (mean number of ova released per mouse) was determined both in a standardized ovulation model in which 25-day-old immature mice were injected with finite amounts of gonadotropins to induce ovulation and during physiological ovulation using adult normally cycling mice. Our results revealed that the temporal onset of follicular wall rupture (first ova observed in bursa or oviduct) was not delayed in plasminogen-deficient mice during gonadotropin-induced ovulation. However, there was a trend toward slightly reduced ovulation efficiency in the plasminogen-deficient mice. This reduction was only 13% and not statistically significant (P = 0.084) and may be connected to a delayed maturation of these mice manifested in reduced body and ovary weights. During physiological ovulation adult plasminogen-deficient mice had normal ovulation efficiency compared with plasminogen wild-type mice. Taken together our results indicate that under the conditions used in this study plasmin is not required for efficient follicular rupture or for activation of other proteases involved in this process. Alternatively, the role of plasmin may be effectively compensated for by other mechanisms in the absence of plasmin.

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