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TE Porter, CE Dean, MM Piper, KL Medvedev, S Ghavam, and J Sandor

Prior research indicates that growth hormone (GH) cell differentiation can be induced prematurely by treatment with glucocorticoids in vitro and in vivo. However, the nature of these responses has not been fully characterized. In this study, the time course of corticosterone induction of GH-secreting cells in cultures of chicken embryonic pituitary cells, responsiveness of differentiated somatotrophs to GH secretagogues, localization of somatotroph precursor cells within the pituitary gland, and the effect of corticosterone on GH gene expression were determined to better define the involvement of glucocorticoids in somatotroph recruitment during development. Anterior pituitary cells from embryonic day 12 chicken embryos were cultured in 10(-9) M corticosterone for 4 to 48 h and were then subjected to reverse haemolytic plaque assays (RHPAs) for GH. Corticosterone treatment for as short as 16 h increased the percentage of GH cells compared with the control. When corticosterone was removed after 48 h and cells were cultured for an additional 3 days in medium alone, the percentage of GH secretors decreased but remained greater than the proportion of somatotrophs among cells that were never treated with corticosterone. To determine if prematurely differentiated somatotrophs were responsive to GH secretagogues, cells were exposed to corticosterone for 48 h and then subjected to GH RHPAs in the presence or absence of GH-releasing hormone (GHRH) or thyrotropin-releasing hormone (TRH). Approximately half of the somatotrophs induced to differentiate with corticosterone subsequently released more GH in response to GHRH and TRH than in their absence. The somatotroph precursor cells were localized within the anterior pituitary by culturing cells from the caudal lobe and cephalic lobe of the anterior pituitary separately. Corticosterone induction of GH cells was substantially greater in cultures derived from the caudal lobe of the anterior pituitary, where somatotroph differentiation normally occurs. GH gene expression was evaluated by ribonuclease protection assay and by in situ hybridization. Corticosterone increased GH mRNA in cultured cells by greater than fourfold. Moreover, corticosterone-induced somatotroph differentiation involved GH gene expression in cells not expressing GH mRNA previously, and the extent of somatotroph differentiation was augmented by treatment with GHRH in combination with corticosterone. We conclude that corticosterone increases the number of GH-secreting cells within 16 h, increases GH gene expression in cells formerly not expressing this gene, confers somatotroph sensitivity to GHRH and TRH, and induces GH production in a precursor population found primarily in the caudal lobe of the anterior pituitary, a site consistent with GH localization in adults. These findings support the hypothesis that glucocorticoids function to induce the final stages in the differentiation of fully functional somatotrophs from cells previously committed to this lineage.

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Mattias Gäreskog and Parri Wentzel

(ROS), which yields mitochondrial swelling and enhanced lipid peroxidation in the embryos. This is because excess pyruvate from glycolysis moves across the mitochondrial membrane, overloading the electron transport chain ( Yang et al. 1998

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Shuai Li and Wipawee Winuthayanon

three major functions: gamete protection, sperm guidance and egg guidance ( Ballester et al. 2014 , Kumaresan et al. 2014 ). After fertilization, the oviduct assists the development of pre-implantation embryos by producing the factors required for

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Stijn L J Van Herck, Stijn Geysens, Edward Bald, Grazyna Chwatko, Evelyne Delezie, Elham Dianati, R G Ahmed, and Veerle M Darras

transferred from the mother to the embryo/foetus, either through the placenta in mammals or through a deposit in the egg in non-mammalian vertebrates, data on the relative MMI concentrations in different embryonic/foetal tissues are scarce. In addition, to

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Anne R O'Connell, Kenneth P McNatty, Peter R Hurst, Thomas E Spencer, Fuller W Bazer, Karen L Reader, Peter D Johnstone, George H Davis, and Jennifer L Juengel

failure of multiple ovulation (PFMO). In cases of PFMO, infertility of the male is excluded because at least one embryo is healthy. It is known that survival of an individual ovum is related to the number of ova ovulated, with ewes ovulating two ova that

Open access

Sara Della Torre, Gianpaolo Rando, Clara Meda, Paolo Ciana, Luisa Ottobrini, and Adriana Maggi

active in most reproductive and non-reproductive tissue cells ( Ciocca & Roig 1995 , Maggi et al. 2004 , Bookout et al. 2006 ). Their expression and transcriptional activity in the course of embryo development is less studied ( Brandenberger et al

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Jiju Wang, Yunhui Tang, Songcun Wang, Liyuan Cui, Dajin Li, and Meirong Du

to induce endometrial decidualization ( Andrade et al. 1996 ); therefore, its influence on the embryo may be ruled out. Further, it was intraperitoneally injected with NE to observe its effect on decidualization. In vitro , primary stromal cells

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Agnieszka Waclawik and Adam J Ziecik

Introduction Maternal recognition of pregnancy requires reciprocal communication between the pre-implantation conceptus (embryo and associated membranes) and maternal system: uterine endometrium and corpus luteum (CL). In the pig

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Shin Tsunekawa, Naoki Yamamoto, Katsura Tsukamoto, Yuji Itoh, Yukiko Kaneko, Toshihide Kimura, Yoh Ariyoshi, Yoshitaka Miura, Yutaka Oiso, and Ichiro Niki

. 1989 ). Briefly, the rat insulin-II promoter/chicken calmodulin cDNA chimeric gene was microinjected into mouse embryos derived from female FVBM mice, followed by the implantation of the embryos into pseudo-pregnant female FVBM mice. The transgenic mice

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Raquel Moral, Richard Wang, Irma H Russo, Coral A Lamartiniere, Julia Pereira, and Jose Russo

exposures, experimental studies in rats, and the US Environmental Protection Agency (US EPA) maximum acceptable dose. Blood sera from human pregnant women have been reported to be 0.46–19 μg/l ( Schonfelder et al . 2002 , Kuroda et al . 2003 , Welshons