Some aspects of regulation of luteal function and luteolysis in equine corpora lutea

Abstract

Like in other mammalian species, in the mare, in every ovarian cycle, a complex process of luteinization leads to corpus luteum (CL) formation. The CL produces progesterone (P4), a required hormone for establishment and maintenance of early pregnancy. Luteal angiogenesis in the mare, necessary for the CL formation, is followed by vascular regression during tissue involution, coordinated with the development and regression of non-vascular tissue (steroidogenic cells included). These processes might be regulated by several factors, still not completely understood. This work reviews some of our studies on this field in the mare. In the equine CL, tumour necrosis factor (TNFα) and nitric oxide (NO) may stimulate the production of angiogenic factor(s) and prostaglandin (PG) E2, necessary for vascular and non-vascular development during the early luteal phase. Increased microvascularization is accompanied by the synthesis of P4, rise in P4 receptor number and an increase in the number of large luteal cells. This suggests the importance of large luteal cells in the auto/paracrine regulation of P4 synthesis in the equine CL. However, when angiogenesis is complete, long term exposure to progestagens appears to inhibit the proliferative/angiogenic activity. PGF2α may also induce luteal (including vascular) regression of the equine CL. Moreover, NO and P4 dependent process of inhibition of angiogenic factor(s) production might be preparing the CL for functional and structural regression. Oppositely to the early luteal phase, during late luteal phase NO and cytokines may induce several processes leading to the regression of equine CL. Besides, caspase-3, the effector enzyme of apoptosis, might also play an important role during luteal tissue involution. Nevertheless, further studies are needed to elucidate the mechanisms and the relationship between the dichotomy of loss of function and/or luteal involution in the mare.