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Distinct Cellular Localization and Regulation of Endothelin-1 and Endothelin-Converting Enzyme-1 Expression in the Bovine Corpus Luteum: Implications for Luteolysis

Department of Animal Sciences (N.L., M.G., R.Ma., R.Me.), Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100, Israel; Howard Hughes Medical Institute and Department of Molecular Genetics (M.Y.), University of Texas, Southwestern Medical Center, Dallas, Texas 75235; and Department of Animal Sciences (M.F.S., J.H.H.), University of Missouri, Columbia, Missouri 65211

Address all correspondence and requests for reprints to: Rina Meidan, Department of Animal Sciences, Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100, Israel. E-mail: rina.meidan{at}huji.ac.il

Endothelin-1 (ET)-1 within the corpus luteum (CL) is rapidly up-regulated during natural or PGF₂-induced luteolysis; however, such an increase was not observed at early luteal stage, when the CL is refractory to PGF₂. The mature and active form of ET-1 is derived from the inactive intermediate peptide, big ET-1, by ET-converting enzyme (ECE)-1. This study therefore examined the developmental and cell-specific expression of ECE-1 in bovine CL. A significant, 4-fold, elevation in ECE-1 expression (mRNA and protein levels) occurred during the transition of the CL from early to midluteal phase. Analysis using in-situ hybridization and enriched luteal cell subpopulations showed that both steroidogenic and endothelial cells of the CL expressed high levels of ECE-1 mRNA; prepro ET-1 mRNA, on the other hand, was only expressed by resident endothelial cells. These data suggest that luteal parenchymal and endothelial cells may cooperate in the biosynthesis of mature bioactive ET-1. In the mature CL, ECE-1 mRNA increase occurred both in steroidogenic and endothelial cells and was accompanied by a significant rise in ET-1 peptide. However, in contrast to ECE-1, prepro ET-1 mRNA levels were similar in early and midluteal-phase CL. Low ECE-1 levels during the early luteal phase, restricting the production of active ET-1, may explain why the immature CL is able to withstand PGF₂-induced luteolysis.

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