Regulation of the porcine corpus luteum during pregnancy

Abstract

The new corpora lutea (CLs) in pigs are formed from the preovulatory follicles after the luteinizing hormone (LH) surge. However, total autonomy and independence of CLs from LH up to Day 12 of cycle has recently been questioned. Transformation of estrous cycle CL to CL of pregnancy initiated by embryonic signals requires not only the cessation of prostaglandin F2 (PGF) supply to the luteal tissue but also needs the CL to overcome luteolytic acquisition and/or changing its sensitivity to PGF during Days 12-14 of pregnancy. The luteolytic cascade is prevented by inhibition of lymphocyte infiltration and leucocyte recruitment, limitation of cell apoptosis, upregulation of pregnancy-associated genes and an enhanced antiluteolytic role of PGE Our 'two-signal switch hypothesis' highlights the importance of PGF and PGE receptor signaling pathways activation in CLs during luteolysis and rescue. The 'luteolytic switch' involves increased expression of many regression mediators and activation of the PTGFR signaling pathway. The 'rescue switch' initiated by embryonic signals - estradiol 17β and PGE - induces PTGER2/4 pathway, turning the 'luteolytic switch' off and triggering activity of genes responsible for CL maintenance. In mid and late pregnancy, CLs are maintained by LH and the synergistic action of metabolic hormones. This paper provides an outline of recent views on CL regression, rescue and maintenance during pregnancy in pigs that conflict with previous paradigms and highlights new findings regarding the actions of prostaglandins, role of microRNAs (miRNA) and immune system and signaling pathways governing the life cycle of porcine CL.

MiRNAs in the Peri-Implantation Period: Contribution to Embryo–Maternal Communication in Pigs

“…In pigs, two main embryonic signals-estradiol-17beta (E2) and prostaglandin E2 (PGE2)-prevent regression of the CL, which occurs on days 13-14 of the estrous cycle. CL rescue is achieved by a paracrine action of the conceptus on the endometrium and the luteal tissue to stop the beginning of luteolysis [1]. Reciprocal communication between the preimplantation conceptus not only results in maintaining P4 production by the ovaries but also sets up the environment for successful embryonic development and implantation.…”

In utero exposure to acetaminophen and ibuprofen leads to intergenerational accelerated reproductive aging in female mice

“…Most PFs remain quiescent, and only few will mature into primary follicles through the coordinated action of various somatic and oocyte factors 26,27 , such as Kit ligand that activates the PI3K/AKT/FOXO3 cascade 28 , a major signalling pathway involved in the regulation of follicle activation and survival 29 . Upon follicle maturation and ovulation, follicular cells differentiate to form the corpus luteum (CL), an endocrine organ that produces progesterone to support pregnancy 30 and that regresses in the absence of pregnancy 31,32 .…”

The Alterations of Endometrial and Myometrial Receptivity in Early Pregnant Gilts in Response to Estrus Induction With PMSG/hCG

“…The PGs are important regulators of the CL lifespan, and PGF2α is responsible for luteal regression in non-pregnant animals [47], while PGE2 functions as a luteotropic and antiluteolytic factor promoting CL maintenance during pregnancy [48]. Additionally, PGs act locally to modulate uterine functions [49,50].…”