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The Molecular Control of Corpus Luteum Formation, Function, and Regression

Department of Obstetrics, Gynecology and Reproductive Science (C.S.), Yale University School of Medicine, New Haven, Connecticut 06510; Division of Basic Biomedical Sciences (C.T.), Sanford School of Medicine of the University of South Dakota, Vermillion, South Dakota 57069; and Department of Physiology and Biophysics (G.G.), University of Illinois College of Medicine, Chicago, Illinois 60612

Correspondence: Address all correspondence and requests for reprints to: Dr. Geula Gibori, Department of Physiology and Biophysics, University of Illinois College of Medicine, 835 South Wolcott Avenue, Chicago, Illinois 60612. E-mail: ggibori{at}uic.edu

The corpus luteum (CL) is one of the few endocrine glands that forms from the remains of another organ and whose function and survival are limited in scope and time. The CL is the site of rapid remodeling, growth, differentiation, and death of cells originating from granulosa, theca, capillaries, and fibroblasts. The apparent raison d’etre of the CL is the production of progesterone, and all the structural and functional features of this gland are geared toward this end. Because of its unique importance for successful pregnancies, the mammals have evolved a complex series of checks and balances that maintains progesterone at appropriate levels throughout gestation. The formation, maintenance, regression, and steroidogenesis of the CL are among the most significant and closely regulated events in mammalian reproduction. During pregnancy, the fate of the CL depends on the interplay of ovarian, pituitary, and placental regulators. At the end of its life span, the CL undergoes a process of regression leading to its disappearance from the ovary and allowing the initiation of a new cycle. The generation of transgenic, knockout and knockin mice and the development of innovative technologies have revealed a novel role of several molecules in the reprogramming of granulosa cells into luteal cells and in the hormonal and molecular control of the function and demise of the CL. The current review highlights our knowledge on these key molecular events in rodents.

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