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This Article Full Text Full Text (PDF) All Versions of this Article: 68/6/2322    most recent biolreprod.102.013540v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Goyeneche, A. A. Articles by Telleria, C. M. Search for Related Content PubMed PubMed Citation Articles by Goyeneche, A. A. Articles by Telleria, C. M. Agricola Articles by Goyeneche, A. A. Articles by Telleria, C. M.

In Vivo Hormonal Environment Leads to Differential Susceptibility of the Corpus Luteum to Apoptosis In Vitro¹

Division of Basic Biomedical Sciences,³ University of South Dakota School of Medicine, Vermillion, South Dakota 57069 Laboratory of Reproduction and Lactation,⁴ IMBECU-CONICET, 5500 Mendoza, Argentina Department of Physiology and Biophysics,⁵ University of Illinois, Chicago, Illinois 60612

We evaluated the involvement of the in vivo hormonal environment on the ability of the rat corpus luteum (CL) to undergo apoptosis. Gel electrophoretic DNA fragmentation analysis revealed no apoptosis in CL isolated either the 2 last days of pregnancy (Days 21 and 22) or throughout the 4 days following parturition, suggesting that the number of cells undergoing apoptosis at the same time is not sufficient to allow for visualization of DNA breakdown. In contrast, CL incubated in serum-free medium underwent significant apoptosis, as evaluated by chromatin condensation and DNA fragmentation, regardless of their developmental stage in pregnancy. However, CL obtained on Day 7 of pregnancy and on Day 4 postpartum demonstrated higher sensitivity to apoptosis in vitro, but lactation reduced significantly the capacity of the CL to undergo apoptosis when maintained in culture. These data suggest that the exposure of the CL to different hormonal environments throughout pregnancy and after parturition is responsible for the differential susceptibility to apoptosis observed in vitro. We have previously shown that progesterone is a direct factor for survival of the CL. Prolactin stimulates luteal progesterone production; therefore, we examined whether prolactin prevents apoptosis in luteal cells independently of its stimulatory action on progesterone production. We used a luteal cell line (GG-CL) that expresses the prolactin receptor but does not produce progesterone. These cells undergo apoptosis under conditions of serum starvation, and addition of prolactin to the culture medium significantly reduced DNA fragmentation. These results indicate that the extent of luteal cell death induced by incubation of CL under serum-free conditions depends on the hormonal environment to which this endocrine gland is exposed in vivo. These results also indicate an important role for lactation in preventing apoptosis, which is further supported by the antiapoptotic activity of prolactin observed in luteal cells.

¹ This research was supported by grants 5 P20 RR16479-02 from NIH/NCRR, HD 11119 from NIH/NICHD, and PICT 1999-05-06877 BID1201-OC AR from the National Agency for Research and Technology of Argentina.

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