Exogenous estradiol enhances apoptosis in regressing post-partum rat corpora lutea possibly mediated by prolactin
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BioMed Central
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Exogenous estradiol enhances apoptosis in regressing post-partum rat corpora lutea possibly mediated by prolactin Alicia A Goyeneche and Carlos M Telleria* Address: Division of Basic Biomedical Sciences, University of South Dakota School of Medicine, Vermillion, South Dakota 57069, USA Email: Alicia A Goyeneche - [email protected]; Carlos M Telleria* - [email protected] * Corresponding author
Published: 30 August 2005 Reproductive Biology and Endocrinology 2005, 3:40
doi:10.1186/1477-7827-3-40
Received: 20 June 2005 Accepted: 30 August 2005
This article is available from: http://www.rbej.com/content/3/1/40 © 2005 Goyeneche and Telleria; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: In pregnant rats, structural luteal regression takes place after parturition and is associated with cell death by apoptosis. We have recently shown that the hormonal environment is responsible for the fate of the corpora lutea (CL). Changing the levels of circulating hormones in post-partum rats, either by injecting androgen, progesterone, or by allowing dams to suckle, was coupled with a delay in the onset of apoptosis in the CL. The objectives of the present investigation were: i) to examine the effect of exogenous estradiol on apoptosis of the rat CL during postpartum luteal regression; and ii) to evaluate the post-partum luteal expression of the estrogen receptor (ER) genes. Methods: In a first experiment, rats after parturition were separated from their pups and injected daily with vehicle or estradiol benzoate for 4 days. On day 4 post-partum, animals were sacrificed, blood samples were taken to determine serum concentrations of hormones, and the ovaries were isolated to study apoptosis in situ. In a second experiment, non-lactating rats after parturition received vehicle, estradiol benzoate or estradiol benzoate plus bromoergocryptine for 4 days, and their CL were isolated and used to study apoptosis ex vivo. In a third experiment, we obtained CL from rats on day 15 of pregnancy and from non-lactating rats on day 4 post-partum, and studied the expression of the messenger RNAs (mRNAs) encoding the ERalpha and ERbeta genes. Results: Exogenous administration of estradiol benzoate induced an increase in the number of apoptotic cells within the CL on day 4 post-partum when compared with animals receiving vehicle alone. Animals treated with the estrogen had higher serum prolactin and progesterone concentrations, with no changes in serum androstenedione. Administration of bromoergocryptine blocked the increase in serum prolactin and progesterone concentrations, and DNA fragmentation induced by the estrogen treatment. ERalpha and ERbeta mRNAs were expressed in CL of day 4 post-partum animals at levels similar to those found i
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