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Progesterone Promotes Survival of the Rat Corpus Luteum in the Absence of Cognate Receptors¹

^a Institute of Medicine and Experimental Biology of Cuyo, LARLAC-CONICET, 5500 Mendoza, Argentina ^b Department of Physiology and Biophysics, University of Illinois, Chicago, Illinois 60612 ^c Department of Morphophysiology, Faculty of Medicine, University of Cuyo, 5500 Mendoza, Argentina

Progesterone production by the corpus luteum (CL) is essential for preparation of the endometrium for implantation and for the maintenance of gestation. Progesterone modulates its own production and opposes functional luteal regression induced by exogenous agents, such as prostaglandin F₂. In the present study, we evaluated whether progesterone is also capable of interfering with the process of structural luteal regression, which is characterized by a decrease in weight and size of the gland because of programmed cell death (i.e., apoptosis). We have found that a low number of luteal cells undergo apoptosis throughout gestation. On the day of parturition, but following the initial decline in endogenous progesterone production, a small increase in the number of luteal cells undergoing cell death was observed. This increase in apoptotic cells continued postpartum, reaching dramatic levels by Day 4 postpartum, and was accompanied by a marked decrease in average luteal weight. We have established that the exogenous administration of progesterone significantly reduces the decline in luteal weight observed during structural luteal regression postpartum. This effect was associated with a decrease in the number of cells undergoing apoptosis and with enhanced circulating levels of androstenedione. Furthermore, in vivo administration of progesterone delayed the occurrence of DNA fragmentation in postpartum CL incubated in serum-free conditions. Finally, we have shown that neither the CL of gestation nor the newly formed CL after postpartum ovulation express the classic progesterone-receptor mRNA. In summary, the present results support a protective action of progesterone on the function and survival of the CL through inhibition of apoptosis and stimulation of androstenedione production. Furthermore, this effect is carried out in the absence of classic progesterone receptors.

¹ Supported by grants from the Ministry of Health, Antorchas Foundation, National Agency for Research, and University of Cuyo, Argentina (C.M.T.); Conicet, Argentina (R.P.D.); and NIH grants FIRCA 1R03 TW01049 (G.G., C.M.T.) and HD11119 (G.G.). Publication costs were supported by the Division of Basic Biomedical Sciences, University of South Dakota.

² Correspondence: Carlos M. Telleria, University of South Dakota School of Medicine, Division of Basic Biomedical Sciences, 414 East Clark Street, Lee Medical & Sciences Building, Vermillion, SD 57069. FAX: 605 677 6381; ctelleri{at}usd.edu

³ Current address: Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, SD 57069

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