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Journal ArticleDOI

Prostaglandin stimulation of in vitro progesterone synthesis.

01 Mar 1970-The Journal of Clinical Endocrinology and Metabolism (The Endocrine Society)-Vol. 30, Iss: 3, pp 345-350
TL;DR: Prostaglandin E2 gave the greatest effect, being approximately half as effective as luteinizing hormone (LH) on a molar basis, and there was no additive effect when prostaglandins were added to luteal slices incubated with saturating doses of either LH or human chorionic gonadotropin (HCG).
Abstract: Bovine corpora lutea slices were incubated with prostaglandins and gonadotropins. All the prostaglandins tested (PGE2, PGE1, PGF2α and PGA1) were found to be steroidogenic, stimulating both the production of progesterone as measured in micrograms and the incorporation of radioactivity from acetate-1-14C. Prostaglandin E2 (PGE2) gave the greatest effect, being approximately half as effective as luteinizing hormone (LH) on a molar basis. There were similarities between gonadotropin and prostaglandin. Cycloheximide (1 mm) equally blocked the steroidogenic response to both PGE2 and LH, the specific activities of the progesterone formed in the presence of prostaglandins and that formed in the presence of gonadotropins were approximately of the same order of magnitude, the time-response curves of PGE2 and LH were similar, and there was no additive effect when prostaglandins were added to luteal slices incubated with saturating doses of either LH or human chorionic gonadotropin (HCG). These results are ...
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Journal ArticleDOI
TL;DR: The uterus can be regarded as a transducer that converts intermittent neural signals from the hypothalamus, in the form of episodic oxytocin secretion, into luteolytic pulses of uterine PGF2alpha, which is a necessary requirement for lutenolysis in ruminants.
Abstract: In many nonprimate mammalian species, cyclical regression of the corpus luteum (luteolysis) is caused by the episodic pulsatile secretion of uterine PGF2α, which acts either locally on the corpus l...

728 citations

Journal ArticleDOI
TL;DR: Indomethacin, an inhibitor of prostaglandin synthesis, blocks ovulation in immature rats pre-treated with pregnant mare serum gonadotropin (PMS), when given either at 0800, 1200 or 1600 hours on the second day after PMS treatment (the equivalent of proestrus in normally cycling adult rats).

263 citations

Book ChapterDOI
TL;DR: The chapter suggests that the number of luteal receptors for LH—but not circulating concentrations of LH—is correlated with serum levels of progesterone throughout the estrous cycle of ewes, and down-regulation of LH receptors depends upon occupancy of the receptor.
Abstract: Publisher Summary This chapter discusses the control of luteal function in domestic ruminant animals. It focuses on data regarding the regulation of receptors for luteinizing hormone (LH) and the characterization of two distinct types of steroidogenic luteal cells. The function of the corpus luteum in ruminants is regulated by a complex interaction of the secretions from at least two other endocrine organs. The adenohypophysis secretes LH, generally accepted as the primary luteotropic hormone in these species. The chapter suggests that the number of luteal receptors for LH—but not circulating concentrations of LH—is correlated with serum levels of progesterone throughout the estrous cycle of ewes. Down-regulation of LH receptors depends upon occupancy of the receptor, based on correlation between number of receptors occupied and number lost after administration of 1 mg of LH in vivo. The major pathway for loss of human chorionic gonadotropin (hCG) or LH bound to the luteal receptor for LH is via internalization and degradation of the hormone. Over 80% of 125I-labeled hCG bound to luteal cells in culture is internalized and degraded. A lesser amount of 125I-labeled LH is internalized and degraded because more of this hormone dissociates from the receptor. A major portion of the internalized population of receptors is recycled to the plasma membrane.

236 citations

Journal ArticleDOI
Frederick A. Kuehl1, John L. Humes1, J. Tarnoff1, V.J. Cirillo1, E. A. Ham1 
28 Aug 1970-Science
TL;DR: Kinetic studies made it possible to suggest that there is a single luteinizing-hormone-related prostaglandin receptor in mouse ovaries, and that activation of this prostag landin receptor is an essential requirement in the action of luteInizing hormone to stimulate adenosine 3',5'-monophosphate formation and steroidogenesis.
Abstract: A dose-response relation was established between prostaglandins and formation of adenosine 39,59-monophosphate in the mouse ovary. The prostaglandin antagonist, 7-oxa-13-prostynoic acid, blocked the stimulatory effect of prostaglandin E 1 , prostaglandin E 2 , and luteinizing hormone on adenosine 39,59-monophosphate formation in a competitive manner. Kinetic studies made it possible to suggest that there is a single luteinizing-hormone-related prostaglandin receptor in mouse ovaries, and that activation of this prostaglandin receptor is an essential requirement in the action of luteinizing hormone to stimulate adenosine 39,59-monophosphate formation and steroidogenesis.

234 citations

Journal ArticleDOI
TL;DR: The purpose of this review is to culminate what is known regarding signal transduction pathways activated by initiator(s) and/or mediators of luteolysis and suggest that the intracellular signaling pathways are key to defining ligand-induced biological responses.
Abstract: The corpus luteum is a unique hormone-regulated, transient reproductive gland that produces progesterone, a required product for the establishment and maintenance of early pregnancy. In the absence of pregnancy the corpus luteum will cease to produce progesterone and the structure itself will regress in size over time. Although the process of luteal regression has been studied for several decades, many of the regulatory mechanisms involved in loss of function and involution of the structure are incompletely understood. More importantly, we are far from understanding how these complex mechanisms function in unison. The factor or factors responsible for initiating and mediating luteolysis are no doubt more complex than originally envisioned. Further, efforts to elucidate the mechanisms responsible for luteolysis have been complicated by different interpretations of what is 'luteolysis', discrepancies between in vitro and in vivo studies, and subsequent biases which are associated with the different methods of analyses. Moreover, the complexity of the mechanisms which regulate the life span of the corpus luteum are compounded by the presence of a heterogeneous population of cells which often respond differentially to the same ligand or stimuli. Attempts to isolate specific luteal cell types for the intention of defining intracellular signaling mechanisms have yielded valuable information. However, studies of a specific cell type taken out of context are often subject to criticism. The most obvious being that the cells are no longer maintained within their three dimensional environment. Evaluation of the corpus luteum in vivo, is not without its criticisms either. A subtle change evoked within a subpopulation of cells can be overlooked if measured in whole tissue or in mixed cell preparations. Furthermore, treatment in vivo with a single agent/ligand (i.e., prostaglandin F2 alpha) may induce a secondary ligand that is ultimately responsible for the biological response. All arguments are valid and cannot be ignored. There are secondary levels of complexity in the corpus luteum brought about by the pleiotropic actions of specific ligands. For example, one ligand can be luteotropic to a steroid producing cell and cytotoxic to a luteal endothelial cell. Furthermore, a specific cell type within the corpus luteum may respond differentially depending on the developmental stage of the luteal phase (i.e., early, mid, or late luteal phase) suggesting that the intracellular signaling pathways are key to defining ligand-induced biological responses. The purpose of this review is to culminate what is known regarding signal transduction pathways activated by initiator(s) and/or mediators of luteolysis. We recognize that an all-inclusive review describing the molecular mechanisms involved in the development, maintenance and regression of the corpus luteum would be impossible within the context of this review. There are a number of recent reviews that discuss luteal development, luteal maintenance and luteolysis with emphasis on neuroendocrine events (1-3). Consequently, we have focused our review primarily on potential intracellular signaling events of proposed regulators and mediators of luteal regression. Where possible we have attempted to incorporate references that represent rodents, domestic farm animals and primates.

207 citations


Cites background from "Prostaglandin stimulation of in vit..."

  • ...3) treatment of luteal tissue with PGF2 alpha in vitro resulted in an acute increase progesterone production (8, 56, 57), 4) PGF2 alpha does not appear to prevent the interaction of LH or IGF-1 (luteotrophic hormones) with...

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