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This paper presents current information on the regulatory mechanism of the endocrine function of the corpus luteum in cyclic and pregnant dogs. Corpus luteum function in the first half of diestrus or pregnancy (< day 30) is independent of gonadotrophins. The mechanisms regulating corpus luteum function in this phase are largely unknown. It seems that an important role in the controlling of progesterone biosynthesis is played by StAR (steroidogenic acute regulatory protein) and 3β-HSD (3β-hydroxysteroid dehydrogenase). Recently, it has been demonstrated that prostaglandin E2 acts luteotrophically by increasing the expression of StAR. In addition, the action of progesterone on its receptors at the para-/autocrine level appears to serve as a luteotrophic factor. There is no significant difference in the regulation of corpus luteum function between pregnant and non-pregnant bitches during this time. Corpus luteum function is fully gonadotrophin-dependent during the second half of diestrus. Prolactin and, to a lesser extent, LH are the main luteotrophic factors. The slow process of luteal regression starts by day 30 after ovulation, and it takes place in spite of the increased availability of pituitary luteotrophic hormones (LH, prolactin). During luteal regression, progesterone concentration gradually decreases. This decrease is caused by a reduced expression of StAR and 3β-HSD, as well as by degenerative changes in the luteal cells. In nonpregnant bitches, progesterone concentration decreases slowly and reaches baseline values 80-90 days after ovulation. In pregnant bitches, on the other hand, progesterone decreases rapidly 1-2 days before parturition. In non-pregnant bitches, luteal regression is a passive process in the absence of luteolytic factors, whereas in pregnant bitches, luteolysis is an active process. This is due to a rapid progesterone decrease to the threshold level and the release of PGF2α from the fetal part of the placenta.
The corpus luteum is an endocrine organ that exhibits extremely rapid growth, development, and regression during the course of each oestrus cycle. At the end of the luteal phase there is an orderly sequence of functional and structural changes in the corpus luteum connected with its regression. This article focuses on selected mechanisms controlling these changes. In these mechanisms, apart from central regulation, the essential role of local monocytes/macrophages and endothelial cells is stressed, as well as intercellular interactions. The research of the last years shows that corpus luteum regression is related to apoptosis. The functional changes that have been initialized by prostaglandin F2 are accompanied by the activation of immunological system cells, which while relieving cytokines work like local regulators in remodeling the corpus luteum. Consequently, metabolic changes, the disappearance of luteal tissue and the final expiration of progesterone production occur.
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