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Journal of the Society for Gynecologic Investigation, Vol. 5, No. 2, 49-57 (1998)
DOI: 10.1177/107155769800500201

Regulation of Luteal Regression: The Ewe as a Model

Patricia B. Hoyer, PhD

Department of Physiology, Arizona Health Sciences Center, University of Arizona, Tueson. AZ 85724 hoyer{at}u.arizona.edu

This articles focuses on mechanisms that regulate functional and structural regression of the regression of the corpus luteum (CL) with special emphasis on the role of prostaglandin F2{alpha} (PGF2{alpha}) in mediating these events in large luteal cells in the ewe. Progesterone produced by the CL is absolutely required in all mammals for implantation and early maintenance of pregnancy. Luteal regression at the end of the nonpregnant cycle involves loss of progesterone production and tissue destruction via physiologic cell death, apoptosis. These are distinct events termed functional and structural regression, respectively. In many mammals, including ewes, luteal regression is initiated by prostaglandin F2{alpha} (PGF2{alpha}) of uterine origin. However, the exact mechanisms of this regulation are not well understood. Functional regression appears to be directly stimulated by PGF2{alpha} via activation of its membrane receptor. Whether structural regression is also initiated directly by PGF2{alpha} is not known. The ovine CL contains two morphologically and functional distinct steroidogenic cell types, designated small and large. Receptors for PGF2{alpha} are exclusively located on large cells. Thus, the signal for regression is received in those cells. These data provide strong evidence that the intracellular determinant of regression resides within the large cell.

Key Words: Lteal regression • prostaglandin F2{alpha} • ovine corpus luteum


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