In this study, we tested the role of colony-stimulating factor 2 (CSF2) as one of the regulatory molecules that mediate maternal effects on embryonic development during the preimplantation period. Our objective was to verify effects of CSF2 on blastocyst yield, determine posttransfer survival, and evaluate properties of the blastocyst formed after CSF2 treatment. In vitro, CSF2 increased the percentage of oocytes that became morulae and blastocysts. Blastocysts that were treated with CSF2 tended to have a greater number of inner cell mass cells and had a higher ratio of inner cell mass to trophectoderm cells. There was no effect of CSF2 on the incidence of apoptosis. Treatment with CSF2 from d 5 to 7 after insemination increased embryonic survival as indicated by improved pregnancy rate at d 30-35 of gestation. Moreover, treatment with CSF2 from either d 1-7 or 5-7 after insemination reduced pregnancy loss after d 30-35. Results indicate that treatment with CSF2 can affect embryonic development and enhance embryo competence for posttransfer survival. The fact that treatment with CSF2 during such a narrow window of development altered embryonic function much later in pregnancy suggests that CSF2 may exert epigenetic effects on the developing embryo that result in persistent changes in function during the embryonic and fetal periods of development.
Dietary sources of fatty acids were evaluated for their influence on oocyte quality and follicular development using 54 lactating cows in summer. Fat supplements were 1) sunflower oil (80% cis 18:1), 2) Ca salt of transoctadecenoic acids (57% trans 18:1), 3) Ca salt of vegetable oils (30% 18:2), and 4) linseed oil (56% 18:3 and 16% 18:2). Fats were fed at 1.35% of dietary dry matter beginning at 5 wk prior to expected calving date and at 1.5% (oils) and 1.75% (Ca salts) of dietary dry matter for 15 wk after parturition. Four days following a programmed induced ovulation, 5 transvaginal oocyte aspirations were performed 3 or 4 d apart. Three days after the last aspiration, PGF2alpha was injected, followed 3 d later by a GnRH injection and a timed artificial insemination (d 0) 16 to 20 h later. For the first 4 aspirations, oocytes grading 1 or 2 were used for in vitro embryo production. Total cell number and the proportion of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive blastomeres were analyzed at d 8. At the fifth aspiration, the occurrence of metaphase II, group II caspase activity, and TUNEL labeling were determined after oocyte maturation. A total of 1,011 oocytes were collected. The proportion of oocytes with high caspase activity was greater for grade 3 compared with grades 1 and 2 (37.5 vs. 1.54 and 1.61%). Feeding polyunsaturated fatty acids, as compared with monosaturated fatty acids, failed to affect oocyte quality, as demonstrated by subsequent embryo development. Cows fed 18:2- or 18:3-enriched diets had a larger preovulatory follicle at insemination and subsequent volume of the corpus luteum compared with those fed cis 18:1 or trans 18:1 diets (16.8, 16.2 vs. 15.0, 14.9 +/- 0.7 mm; 7,323, 8,208 vs. 6,033, 5,495 +/- 644 mm3, respectively). The previously documented benefits of polyunsaturated fatty acids on reproductive performance appear to reflect actions at alternative biological windows in lactating dairy cows.
Successful embryonic development is dependent on factors secreted by the reproductive tract. Dickkopf-1 (DKK1), an antagonist of the wingless-related mouse mammary tumor virus (WNT) signaling pathway, is one endometrial secretory protein potentially involved in maternal-embryo communication. The purpose of this study was to investigate the roles of DKK1 in embryo cell fate decisions and competence to establish pregnancy. Using in vitro-produced bovine embryos, we demonstrate that exposure of embryos to DKK1 during the period of morula to blastocyst transition (between d 5 and 8 of development) promotes the first 2 cell fate decisions leading to increased differentiation of cells toward the trophectoderm and hypoblast lineages compared with that for control embryos treated with vehicle. Moreover, treatment of embryos with DKK1 or colony-stimulating factor 2 (CSF2; an endometrial cytokine known to improve embryo development and pregnancy establishment) between d 5 and 7 of development improves embryo survival after transfer to recipients. Pregnancy success at d 32 of gestation was 27% for cows receiving control embryos treated with vehicle, 41% for cows receiving embryos treated with DKK1, and 39% for cows receiving embryos treated with CSF2. These novel findings represent the first evidence of a role for maternally derived WNT regulators during this period and could lead to improvements in assisted reproductive technologies.
Uterine contamination with bacteria is ubiquitous in the postpartum dairy cow. Nearly one-half of all postpartum dairy cows develop clinical disease resulting in metritis and endometritis, which cause depressed milk production and infertility. The causative links between uterine infection and infertility include a hostile uterine environment, disrupted endocrine signaling, and perturbations in ovarian function and oocyte development. In this review we consider the various mechanisms linking uterine infection with infertility in the dairy cow, specifically 1) innate immune signaling in the endometrium, 2) alteration in endocrine signaling in response to infectious agents, and 3) impacts of infection on ovarian function, oocyte development, and follicular development. Normal ovarian follicular and oocyte development requires a series of temporally and spatially orchestrated events; however, several of the cellular pathways required for ovarian function are also used during the innate immune response to bacterial pathogens. We propose that activation of cellular pathways during this immune response has a negative impact on ovarian physiology, which is manifest as infertility detected after the clearance of the bacteria. This review highlights how new insights into infection and immunity in cattle are linked to infertility.
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