Cl Maintenance

The timing and strength of embryonic signals probably allow the mother to evaluate the fitness of a conceptus and to terminate a pregnancy before investment is too high. Embryos that possess chromosomal abnormalities, that are developmentally stunted, or are suffering setbacks as the result of detrimental environmental and nutritional conditions in the uterus, are likely to be delayed in their development and to signal less than robustly to the mother.[1,2] Accordingly, deficient MRP signaling probably underpins much of the early embryonic loss that occurs in the first three weeks of pregnancy.

In early pregnancy, the CL is the major source of progesterone, a steroid hormone that acts on the endometrium to maintain it in a state whereby it remains receptive and provides nourishment to the embryo.[3,4] Two strategies are principally employed by conceptuses to avoid a return to cyclicity: the production of either a luteotrophic signal that promotes CL growth and activity or an antiluteolytic signal that protects the CL.[3] There are examples, e.g., dogs and marsupials, where no intervention is needed because the duration of pregnancy corresponds to the length of the luteal phase of the estrous cycle. The estrous cycles of livestock are short compared to pregnancy so that CL rescue is required.[2,5,6]

In all livestock, luteolysis is initiated by prostaglandin F2a (PGF2a) produced in the endometrium (the lining of the uterus) toward the end of the cycle.[7] PGF2a reaches the ovary via maternal blood, and, by mechanisms still not completely clear, causes the structural and functional demise of the progesterone-producing luteal cells. In some species, oxytocin has a role in initiating PGF2a release from the endometrium.[7] Conceptuses ensure CL lifespan extension by either intervening in the production and/or release of PGF2a, counteracting its actions at the level of the ovary, or by a combination of strategies.[3,9]

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