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Figure 2 | Reproductive Biology and Endocrinology

Figure 2

From: Regulation of intraluteal production of prostaglandins

Figure 2

A model for the regulation of PG production during different stages of luteal differentiation. In the granulosa cell of the preovulatory follicle there is very low PG production and low expression of Cox-2. The LH surge induces Cox-2 expression through the protein kinase A (PKA) pathway but with a delay in expression depending upon the species [83]. In the early luteal cell there is high PG production that is stimulated by pathways that have not yet been defined. It is also possible that high Cox-2 protein has been left after the dramatic induction of Cox-2 after the LH surge. In the early luteal cell and in the CL without luteolytic capacity (these 2 stages may overlap), there are PGF receptors but PGF does not stimulate increased intraluteal PG production (shown by red lines). In addition, PGF does not induce other activators of PG production, such as decreased progesterone secretion, increased endothelin-1 production, or increased cytokine production. Unknown mechanisms cause the CL to acquire luteolytic capacity. After acquisition of luteolytic capacity, treatment with PGF increases intraluteal PG production. Activation of cytosolic phospholipase A2 (cPLA2) by increased free intracellular calcium concentrations provides arachidonic acid (A.A.) substrate to the induced Cox-2 enzyme. Although not shown, these events are likely to be localized to the nuclear membrane. Intraluteal PGF production activates an autoamplification loop in the mature CL due to PGF-induced Cox-2 expression and PGF induction of other activators of Cox-2 expression.

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