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D. SCHAMS, B. HOFFMANN, S. FISCHER, E. MARZ and H. KARG

Summary.

Levels of lh were determined by radioimmunoassay and those of progesterone by a competitive protein-binding technique. Blood samples from eight cows, representing two complete pregnancies (including post-partum periods), and from one cow in the first trimester and another around the time of parturition, were collected. The samples were withdrawn at intervals of 6 hr for lh and every 4 to 5 days for progesterone determination. Levels of lh were consistently low (1·0 to 1·6 ng/ml plasma) with a few single peaks occurring irregularly in individuals during the first 110 days. Distinct lh peaks were observed between Days 7 and 20 post partum. The decrease of progesterone from high levels during pregnancy (plateau between 5 and 9 ng/ml plasma with individual differences) before parturition and the low level following was not reflected in the lh concentration. In an experiment with one animal, an injection of 5 mg flumethasone near term caused a partial decrease in the progesterone concentration, and a larger dose of 10 mg induced parturition. This was preceded by a marked decrease of progesterone similar to that observed before a normal delivery.

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W. Schlegel, S. Krüger, D. Daniels, B. Fischer, H. P. G. Schneider and H. M. Beier

Summary. Corpora lutea and ovarian stromal tissue were anlaysed for prostaglandin (PG) concentrations and activities of enzymes involved in PG metabolism at 8, 10, 12, 13 and 15 days after induction of ovulation. In CL of pseudopregnant rabbits, the PGE-2–9-ketoreductase (PGE-2–9-KR) was highly active on Days 10, 12 and 15 when compared with Day 8 (P < 0·01; P < 0·001; P < 0·05). In pregnant animals PGE-2–9KR activity was only increased on Day 12 (P < 0·05) but declined to basal levels on Days 13 and 15. Comparing PGE-2–9-KR activity of pseudopregnant and pregnant animals, a significant elevation was found on Day 15 of pseudopregnancy (P < 0·025). Activities of PG-15-hydroxydehydrogenase did not exhibit any significant changes with time in pseudopregnant or pregnant rabbits.

PGE-2 concentrations were increased on Days 12, 13 and 15 (P < 0·025) when compared with Day 8. Changes in PGF-2α concentrations paralleled those of PGE-2–9-KR. The concentrations of PG metabolites 13,14-dihydro-15-keto-PGE-2 and -PGF-2α were lower than those of the primary PGs and did not show stage-specific changes in pseudopregnant and pregnant animals.

These results demonstrate that the rabbit CL posesses enzymes to convert PGE-2 to PGF-2α and to metabolize both PGs. PGE-2–9-KR may be involved in regulating the PGF-2α/PGE-2 ratio and possibly in controlling the life-span of the corpus luteum.

Keywords: PGE-2-9-ketoreductase; prostaglandin-15-hydroxydehydrogenase; luteolysis; prostaglandin metabolism; pseudopregnancy; rabbit

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P Pocar, B Fischer, T Klonisch and S Hombach-Klonisch

The dioxin/aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor responsive to both natural and man-made environmental compounds. AhR and its nuclear partner ARNT are expressed in the female reproductive tract in a variety of species and several indications suggest that the AhR might play a pivotal role in the physiology of reproduction. Furthermore, it appears to be the mediator of most, if not all, the adverse effects on reproduction of a group of highly potent environmental pollutants collectively called aryl hydrocarbons (AHs), including the highly toxic compound 2,3,7,8-tetrachlor-odibenzo-p-dioxin (TCDD). Although a large body of recent literature has implicated AhR in multiple signal transduction pathways, the mechanisms of action resulting in a wide spectrum of effects on female reproduction are largely unknown. Here we summarize the major types of molecular cross-talks that have been identified for the AhR and linked cell signaling pathways and that are relevant for the understanding of the role of this transcription factor in female reproduction.

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D M Baston-Buest, A Schanz, S Buest, J C Fischer, J S Kruessel and A P Hess

A successful implantation of a mammalian embryo into the maternal endometrium depends on a highly synchronized fetal–maternal dialogue involving chemokines, growth factors, and matrix-modifying enzymes. A growing body of evidence suggests an important role for proteinases playing a role in matrix degeneration and enhancing the embryo's invasive capacity and influencing the mother's immunological status in favor of the conceptus. This study focused on the expression of cathepsin S (CTSS) and its inhibitors in the murine fetal–maternal interface as well as the detection of the cellular sources of either proteinase and inhibitors. Nested RT-PCR for detection of embryonic mRNAs, immunohistochemistry of maternal and fetal tissues in B6C3F1 mice, and FACS analysis for determination of immunocompetent cell population were applied. This study shows that the cysteine proteinase CTSS is upregulated in the stroma of the implantation site, and that pregnancy induces an influx of CTSS-positive uterine natural killer cells. Compared to maternal tissues, the CTSS inhibitors cystatin F and C, but not the proteinase itself, are expressed in blastocysts. In conclusion, CTSS underlies a hormonal regulation in the maternal tissue and therewith most likely supports the embryonic implantation. The invading embryo regulates the depth of its own invasion through the expression of the cathepsin inhibitors and furthermore, interleukin-6 to activate CTSS in maternal tissues. Additionally, the observed decrease in CD3+ cells leads to the hypothesis that cells of the cytotoxic T-cell group are down-regulated in the decidua to support the implantation and ensure the survival of the embryo.

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C. S. Asa, E. W. Houston, M. T. Fischer, J. E. Bauman, K. L. Bauman, P. K. Hagberg and B. W. Read

Changes in serum oestradiol and progesterone were measured to study their dynamics during ovulatory cycles in six female addax, an endangered antelope. Blood was collected three times per week, during chute restraint, for 3 months (November to February) before introduction of a male, and continued until pregnancy was diagnosed with ultrasound. Serum was analysed by enzymeimmunoassay. Mean luteal phase, interluteal phase, and cycle durations were 22.7 ± 2.0, 8.78 ± 0.5 and 32.3 ± 1.7 days, respectively. Ultrasonography revealed coiled uterine horns and maximum follicle and corpus luteum diameters of 15 and 27 mm, respectively. Each female experienced an anovulatory period, during which oestradiol continued to fluctuate, but progesterone remained below 2 ng ml−1. These periods ranged from 39 to 131 days and were not synchronous; ovulatory cycles resumed spontaneously in all females. All four females placed with a male conceived. Because addax give birth all year round, they are not considered seasonal breeders. The sporadic periods of anovulation that occurred during the winter months of this study suggest a possible seasonal effect. However, systematic sampling has not been conducted during summer and early autumn and will be necessary to address this question.

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Jacqueline Gürke, Maria Schindler, S Mareike Pendzialek, René Thieme, Katarzyna J Grybel, Regine Heller, Katrin Spengler, Tom P Fleming, Bernd Fischer and Anne Navarrete Santos

The mammalian target of rapamycin complex 1 (mTORC1) is known to be a central cellular nutrient sensor and master regulator of protein metabolism; therefore, it is indispensable for normal embryonic development. We showed previously in a diabetic pregnancy that embryonic mTORC1 phosphorylation is increased in case of maternal hyperglycaemia and hypoinsulinaemia. Further, the preimplantation embryo is exposed to increased L-leucine levels during a diabetic pregnancy. To understand how mTOR signalling is regulated in preimplantation embryos, we examined consequences of L-leucine and glucose stimulation on mTORC1 signalling and downstream targets in in vitro cultured preimplantation rabbit blastocysts and in vivo. High levels of L-leucine and glucose lead to higher phosphorylation of mTORC1 and its downstream target ribosomal S6 kinase 1 (S6K1) in these embryos. Further, L-leucine supplementation resulted in higher embryonic expression of genes involved in cell cycle (cyclin D1; CCND1), translation initiation (eukaryotic translation initiation factor 4E; EIF4E), amino acid transport (large neutral amino acid transporter 2; Lat2: gene SLC7A8) and proliferation (proliferating cell nuclear antigen; PCNA) in a mTORC1-dependent manner. Phosphorylation of S6K1 and expression patterns of CCND1 and EIF4E were increased in embryos from diabetic rabbits, while the expression of proliferation marker PCNA was decreased. In these embryos, protein synthesis was increased and autophagic activity was decreased. We conclude that mammalian preimplantation embryos sense changes in nutrient supply via mTORC1 signalling. Therefore, mTORC1 may be a decisive mediator of metabolic programming in a diabetic pregnancy.

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J Burkuš, A Navarrete Santos, M Schindler, J Babeľová, J S Jung, A Špirková, M Kšiňanová, V Kovaříková, B Fischer, J Koppel, D Fabian and Š Čikoš

Preimplantation embryos are sensitive to maternal hormones affecting embryonic signal transduction and metabolic functions. We examined whether adiponectin, the most abundantly secreted adipokine, can influence glucose transport in mouse embryonic cells. In mouse blastocysts full-length adiponectin stimulated glucose uptake, while no effect of globular adiponectin was found. Full-length adiponectin stimulated translocation of GLUT8 glucose transporter to the cell membrane; we did not detect significant changes in the intracellular localization of GLUT4 glucose transporter in adiponectin-treated blastocysts. To study adiponectin signaling in detail, we used embryoid bodies formed from mouse embryonic carcinoma cell (ECC) line P19. We confirmed the expression of adiponectin receptors in these cells. Similar to mouse blastocysts, full-length adiponectin, but not globular adiponectin, stimulated glucose uptake in ECC P19 embryoid bodies. Moreover, full-length adiponectin stimulated AMPK and p38 MAPK phosphorylation. These results indicate that besides AMPK, p38 MAPK is a potential target of adiponectin in mouse embryonic cells. AMPK inhibitor did not influence the adiponectin-stimulated p38 MAPK phosphorylation, indicating independent action of these two signaling pathways. In mouse embryos adiponectin acts as a hormonal regulator of glucose uptake, which becomes especially important in phases with reduced levels of circulating insulin. Our results suggest that adiponectin maintains the glucose supply for early embryos under hypoinsulinaemic conditions, for example, in mothers suffering from type 1 diabetes mellitus.