Current Knowledge on the Multifactorial Regulation of Corpora Lutea Lifespan: The Rabbit Model

Abstract

Our research group studied the biological regulatory mechanisms of the corpora lutea (CL), paying particular attention to the pseudopregnant rabbit model, which has the advantage that the relative luteal age following ovulation is induced by the gonadotrophin-releasing hormone (GnRH). CL are temporary endocrine structures that secrete progesterone, which is essential for maintaining a healthy pregnancy. It is now clear that, besides the classical regulatory mechanism exerted by prostaglandin E2 (luteotropic) and prostaglandin F2α (luteolytic), a considerable number of other effectors assist in the regulation of CL. The aim of this paper is to summarize our current knowledge of the multifactorial mechanisms regulating CL lifespan in rabbits. Given the essential role of CL in reproductive success, a deeper understanding of the regulatory mechanisms will provide us with valuable insights on various reproductive issues that hinder fertility in this and other mammalian species, allowing to overcome the challenges for new and more efficient breeding strategies.

Keywords: corpus luteum; rabbit; reproduction.

Figure 1

Schematic model reporting the functional (upper) and structural (lower) luteolytic pathways induced by prostaglandin F2 α (PGF2α) in rabbit mid-corpora lutea (CL) (day 9 of pseudopregnancy). Since prostaglandin E2 (PGE2)-9-K and 20α-hydroxysteroid dehydrogenase (HSD) represent two different activities of a single enzyme, they are joined. Figure from the study by Maranesi et al. 2010 [31]. For acronyms, see the list of abbreviations in the text.

Figure 2

Schematic representation of the leptin mechanisms regulating progesterone release in rabbit mid-CL. For acronyms, see the list of abbreviations in the text.

Figure 3

Schematic representation of the post-receptorial mechanism of GnRH-I regulating the progesterone release in rabbit CL. The other possible protein kinase C (PKC) targets are represented by hatched lines. Figure from the study by Zerani et al. 2010 [85]. For acronyms, see the list of abbreviations in the text.

Figure 4

Schematic diagram of the adrenocorticotropic hormone (ACTH), kisspeptins (KiSS) and peroxisome proliferator-activated receptor (PPAR) mechanisms modulating progesterone release in early rabbit CL. The effectors that could directly modulate the KiSS/KiSSR (receptor) system at the CL level are represented by blue lines. For acronyms, see the list of abbreviations in the text.

Figure 5

Schematic representation of the dopamine receptor-dependent mechanism modulating progesterone production in early (Day 4) and late (Day 9) rabbit CL. D1R: dopamine receptor subtype 1 (cAMP increase) and D3R: dopamine receptor subtype 3 (cAMP decrease). Italic: D1R and D3R genes. Figure from the study by Parillo et al. 2014 [132].