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Results for “Embryo Implantation, Delayed”

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PubMed1982

A study of carbohydrate metabolism in 'delayed' and 'activated' mouse blastocyst and uterus.

Several regulatory enzymes of carbohydrate metabolism were studied in blastocysts and uteri of mice in which implantation had been delayed and of oestrogen-activated mice, and compared with those of normal mice just before implantation on day 4 of pregnancy. A significant increase in the activities of phosphofructokinase and pyruvate kinase was observed but the level of lactate dehydrogenase declined in delayed blastocysts. Carbohydrate metabolism in the uterus remained essentially unchanged during the delay period. A study of uterine mitotic patterns showed a steady increase in stromal mitosis after administration of oestradiol to animals in which implantation had been delayed.

Animals↗
PubMed1990

Ovarian stimulation protocol for in vitro fertilization with gonadotropin-releasing hormone agonist widens the implantation window.

Pregnancy rates vary considerably with the type of ovarian stimulation used for in vitro fertilization and embryo transfer (IVF-ET). The window of implantation may represent one of the rate-limiting steps in IVF success. We therefore investigated estimated implantation times of 10 consecutive IVF singleton pregnancies, achieved using pituitary suppression with gonadotropin-releasing hormone agonist (GnRH-a) before and during ovarian stimulation with human menopausal gonadotropins (hMG), and compared those with 9 consecutive IVF pregnancies achieved by hMG stimulation only. Estimated implantation times were calculated by regression analysis of serial human chorionic gonadotropin (hCG) measurements between days 7 and 16 after ET. The GnRH-a/hMG pregnancies implanted between days 7 and 11, whereas hMG pregnancies implanted between days 7 and 9 after ET. The hCG regression curve for the GnRH-a/hMG pregnancies revealed a delay of 1.5 days in estimated implantation time compared with the hMG only group. There were no significant differences in pretransfer in vitro embryos development between the two groups. Thus, the delay in hCG rise probably reflects a delay in embryo implantation. We therefore conclude that a GnRH-a/hMG stimulation protocol appears to widen the implantation window in comparison with a hMG only protocol. This observation may at least in part explain the improved IVF pregnancy success with GnRH-a/hMG stimulation protocols.

Chorionic Gonadotropin↗
PubMed1981

Activation of amino acid accumulation in delayed implantation mouse blastocysts.

Delayed implantation blastocysts remained in a diapausing-like state when incubated in Na+ -depleted (55 mM) medium. Accumulation of radioactive amino acids remained low when embryos were in low Na+ medium, but increased in the manner characteristic of these embryos when placed in high (124 mM) Na+ medium. Differentiation of blastocysts was apparently arrested in medium containing only 55 mM Na+ since no progress toward formation of trophoblastic outgrowths was made in this medium even when it contained all other compounds required for this process. Low Na+ may prevent uptake of amino acids, such as lysine, essential to outgrowth formation. Accumulation of lysine was Na+ -dependent in blastocysts even though this amino acid is not transported via a Na+-symport system in most cell types. Glucose deprivation did not affect the increase in the capacity of delayed implantation blastocysts to take up amino acids when incubated in high Na+ medium, and glucose accumulation was not Na+-dependent. The capacity of delayed implantation blastocysts to take up amino acids was inversely related to the time before these embryos began forming outgrowths in vitro. The latter process occurred more rapidly if diapausing blastocysts had been stimulated in utero by injecting overiectomized mice with progesterone and estrogen. However, these hormones slowed outgrowth formation slightly when present in the culture medium in vitro.

Amino Acids↗
PubMed1981

Cytology of the endometrium of delayed and early implantation with special reference to mice and mustelids.

Although it is apparent that the uterus is involved in the control of embryonic diapause, in no instance do we know the precise nature of that control. The most direct control would be through synthesis of proteins or other macromolecules by the uterus itself. Whereas luminal contents have been shown to vary significantly near the time of implantation, neither the role of the luminal fluid constituents, nor the cellular origins of these molecules are fully known, nor have the mechanisms of storage and secretion of proteins in the endometrium been fully established. Cellular structures that may be indicative of functional activity include secretory granules or vesicles, increase or dilation of granular endoplasmic reticulum and increase in size, and associated vesicles of the Golgi complex. Storage of glycogen or lipid appears more indicative of lowered activity. However, despite striking changes in these cytological characteristics in different animals during delay and early implantation, there is no single pattern during the delay period, and no predictable alteration in the peri-implantation period. In general, the structure of the uterus of an animal during delay resembles a modification of that of a closely related species that does not delay more than it resembles that of other species that do show delay.

Animals↗
PubMed2005

LPA3-mediated lysophosphatidic acid signalling in embryo implantation and spacing.

Every successful pregnancy requires proper embryo implantation. Low implantation rate is a major problem during infertility treatments using assisted reproductive technologies. Here we report a newly discovered molecular influence on implantation through the lysophosphatidic acid (LPA) receptor LPA3 (refs 2-4). Targeted deletion of LPA3 in mice resulted in significantly reduced litter size, which could be attributed to delayed implantation and altered embryo spacing. These two events led to delayed embryonic development, hypertrophic placentas shared by multiple embryos and embryonic death. An enzyme demonstrated to influence implantation, cyclooxygenase 2 (COX2) (ref. 5), was downregulated in LPA3-deficient uteri during pre-implantation. Downregulation of COX2 led to reduced levels of prostaglandins E2 and I2 (PGE2 and PGI2), which are critical for implantation. Exogenous administration of PGE2 or carbaprostacyclin (a stable analogue of PGI2) into LPA3-deficient female mice rescued delayed implantation but did not rescue defects in embryo spacing. These data identify LPA3 receptor-mediated signalling as having an influence on implantation, and further indicate linkage between LPA signalling and prostaglandin biosynthesis.

Animals↗