POLYAMINE REGULATION OF PROGESTERONE BIOSYNTHESIS

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The corpus luteum is a transient endocrine gland, which forms on the ovary at the site of ovulation. Synthesis and secretion of the steroid hormone, progesterone, by the corpus luteum is requisite for the establishment of normal reproductive cycles and maintenance of pregnancy in females. We have convincing data suggesting that the aliphatic organic cations known as polyamines, effect progesterone secretion by the corpus luteum. Polyamines are ubiquitously are ubiquitously distributed throughout mammalian cells where they are involved in a multitude of cellular functions include cell proliferation, transcription, translation, hormone receptor-ligand binding, second messenger levels and enzymatic activities. In addition to the roles of polyamines in normal cellular functions, increased polyamine metabolism is associated with malignant cell proliferation. Although polyamines play pivotal roles in normal and abnormal cellular function, their role in ovarian regulation, specifically corpus luteum steroidogenesis has not been evaluated. The overall goal of this investigation is to determine the role of polyamines in progesterone synthesis and secretion by the corpus luteum. Our immediate aims are to determine if polyamines 1) influence accumulation of mRNA for steroidogenic enzymes, 2) influence accumulation of mRNA for proteins involved in cholesterol transport, 3) alter levels of mRNA encoding oxidative stress response enzymes, and 4) effect prostaglandin F/2alpha signal transduction pathways. These experiments will provide information regarding intracellular mechanisms which govern steroidogenic mechanisms within the ovary. By conducting these experiments, we anticipate making significant contributions toward understanding the role of polyamines in ovarian steroidogenesis. By conducting both in vivo and in vitro experiments which utilizes molecular methodologies we are confident these aims will be accomplished and provide new insight into ovarian mechanisms that control steroidogenesis.