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Results for “Embryo Implantation, Delayed”

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PubMed1983

Inhibitory influence of uterine secretions on mouse blastocysts decreases at the time of blastocyst activation.

Uterine flushings from artificially 'pseudopregnant', pseudopregnant and pregnant mice and those with 'diapausing' embryos were tested for their effect on [3H]uridine incorporation by mouse blastocysts. An inhibitor of [3H]uridine incorporation was detected in the uterine fluid of the mice with diapausing embryos and the activity of the inhibitor was significantly reduced 6.25 h after an injection of oestrogen. This reduction of the inhibitory activity was dependent on the presence of blastocysts in utero, since a similar reduction did not occur in uterine fluids of pseudopregnant mice. The results support the suggestion that 'delayed' implantation in mice is caused by the presence of inhibitors of blastocyst metabolism and that activation, after an increase in oestradiol, is due to an embryo-dependent loss of activity of the inhibitors.

Animals↗
PubMed1985

The glycocalyx of the mouse uterine luminal epithelium during estrus, early pregnancy, the peri-implantation period, and delayed implantation. I. Acquisition of Ricinus communis I binding sites during pregnancy.

Mouse uteri were examined during estrus, early pregnancy, the peri-implantation period, and delayed implantation to determine whether changes in the surface coat of the luminal epithelium could be associated with receptivity of the uterus to the presence of blastocyst-stage embryos or blastocyst adhesion. By using alkaline bismuth subnitrate to label periodate-oxidized glycols within the glycocalyx we were able to measure the thickness and examine the morphology of the glycocalyx by electron microscopy. Ferritin-conjugated Ricinus communis agglutinin (RCA-I) demonstrated the presence of D-galactose at terminal, nonreducing positions within the glycocalyx. A relatively thick (0.06-0.1-micron) surface coat was present during estrus, but contained almost no RCA-I binding sites. During Day 3 of pregnancy the surface coat remained up to 0.1 micron thick and RCA-I binding sites were present. At Day 4 and during delay the glycocalyx had a fibrillar appearance, contained RCA-I binding sites, and was reduced to 0.06-0.08 micron in thickness. During Day 5 of pregnancy the thickness of the surface coat was greatly reduced, but there remained uniform lectin binding adjacent to the plasma membrane both at sites of blastocyst attachment and between implantation sites. The results indicate that the luminal epithelium of the mouse uterus acquired RCA-I binding sites during pregnancy and that the thickness of the surface coat was greatly reduced at the time of implantation.

Animals↗
PubMed1979

Scanning electron microscopy of the surface of normal and implantation-delayed mouse blastocysts during development in vitro.

Mouse blastocysts undergo developmental steps in culture analogous to those occurring during implantation in utero. We examined cultured blastocysts by scanning electron microscopy (SEM) as they passed through these stages. From the time of hatching to the acquisition of adhesiveness, most blastocysts were exhanded, with flattened cells possessing relatively small numbers of microvilli, centrally raised areas (presumably reflecting the location of the nuclei) and intercellular ridges often possessing microvilli. At, or shortly before, the trophoblast outgrowth stage, blastocysts appeared to contract; the cells bulged noticeably, microvilli covered the entire surface of most cells and intercellular ridges were no longer observable. Blastocysts removed from uteri on the seventh day of ovariectomy delay possessed a variety of morphologies and shapes. The blastocoel was frequently collapsed and cell outlines were difficult to discern. These blastocysts were initially adhesive in vitro, but subsequently disengaged from the substratum before becoming permanently adherent several hours later. During the initial phase of adhesiveness, blastocysts were elongated and had prominent intercellular ridges, particularly in the equatorial region. Detached blastocysts contained bulging cells with contours which obscured the intercellular ridges. Surface ultrastructure during subsequent phases resembled non-delayed blastocysts during attachment and outgrowth. On the basis of our studies, we propose that intercellular ridges play some role in blastocyst adhesiveness. However, we must conclude that there are other factors involved in the acquisition of adhesiveness by the blastocyst which are at least equally important but of a nature too subtle to be identified by our SEM analyses. Insofar as delayed blastocysts are concerned, we find that, within limits, the surface alterations that take place when blastocysts are activated in culture mirror those observed following reversal of delay in vivo by administration of hormones. Since delayed blastocysts placed in saline also undergo morphological changes resembling those seen at the onset of activation in utero, we suggest that reversal of implantation delay requires initially neither direct contact with steroid or macromolecular inducers nor an exogenous supply of metabolites.

Adhesiveness↗
PubMed1983

Sodium ion concentrations in uterine flushings from "implanting" and "delayed implanting" mice.

The uteri of mice were flushed with isotonic mannitol (1) on the day of implantation during normal pregnancy or (2) during delay of implantation. The Na+ concentration in flushings was reduced during diapause but had increased by 65% 24 h after progesterone-treated ovariectomized mice received estrogen injections. The results suggest that the apparent metabolic quiescence of diapausing blastocysts may, in part, be a consequence of lower (Na+) in the uterus during delay of implantation.

Animals↗
PubMed1984

Presence of an inhibitor of plasminogen activator in uterine fluid of the western spotted skunk during delayed implantation.

This study was designed to test the hypothesis that protease inhibitors would be present in uterine fluids of the western spotted skunk during the period of delayed implantation but would decline or disappear during implantation. Blood plasma, uterine flushings and medium from endometrial cultures were collected 40-70 days preimplantation (Stage 1), 20-25 days preimplantation (Stage 2), 1-3 days preimplantation (Stage 3) and 1-5 days postimplantation (Stage 4). Protein content of the flushings was low in Stage 1 (12.9 +/- 3.0 micrograms), increased slightly (21.8 +/- 6.4 micrograms) during Stage 2 and increased markedly in Stages 3 (99 +/- 44.8 micrograms) and 4 (256 +/- 150 micrograms). No protease activity was detected in any fluid at any stage. Uterine flushings, however, contained an inhibitor of plasminogen activator (PA) of apparent molecular weight approximately 70,000. The total amount of inhibitor increased as pregnancy progressed, but specific inhibitory activity was highest during Stages 1 and 2 (1.7 and 3.2 units/micrograms protein, respectively) and declined in Stages 3 and 4 (1.2 and 0.6 units/micrograms protein, respectively). The inhibitor was present in medium from uterine cultures but was low in plasma. All of the fluids could inhibit trypsin, but not plasmin. The antitrypsin activity in uterine fluids is attributed to plasma transudate. The results demonstrate an inhibitor of PA in skunk uterine fluids but show no temporal relationship between its presence and the period of obligate delay of implantation.

Animals↗
PubMed1993

Contrasting action of antiestrogen (ICI-182780) for preventing initiation of embryo implantation by estradiol or epidermal growth factor (EGF).

The pure estrogen antagonist ICI-182780, at doses above 50 micrograms/kg, effectively inhibited the initiation of embryo implantation in rats when administered on day 4 of pregnancy (day 1 = sperm positive). The same dose inhibited the implantation initiating effect of intravenous 25 ng of estradiol-17 beta in delayed implanting progesterone-primed hypophysectomized rats. In contrast, the anti-estrogen at a dose of 1 mg/kg was ineffective at inhibiting the initiation of implantation induced by intrauterine plus intravenous administration of murine epidermal growth factor to delayed implanting rats. The growth factor also initiated implantation of blastocysts transferred from donor animals injected with the anti-estrogen to progesterone-primed hypophysectomized recipients. The results clearly demonstrate that the implantation initiating effect of the growth factor is not inhibited by a pure estrogen antagonist, and therefore this estrogenic function does not appear to require action initiated by the classical estrogen receptor.

Animals↗