Estrogen synthesis and metabolism in the hamster blastocyst, uterus and liver near the time of implantation

Sholl, Samuel A.; Orsini, Margaret Ward; Hitchins, David J.

doi:10.1016/0022-4731(83)90410-7

Cited by 25 publications

(9 citation statements)

References 24 publications

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“…A hypothesis has been proposed that blastocysts in these species could synthesize and secrete estrogen locally to initiate implantation (Dey et al, 2004; Wang and Dey, 2006). In agreement with this, aromatase, an enzyme for estrogen synthesis, is detected in the blastocyst of hamster and rabbit, while such an aromatase is absent in mice (Dickmann et al, 1975;Hoversland et al, 1982a; Reese et al, 2008; Sengupta et al, 1983; Sholl et al, 1983). It remains unclear whether blastocyst-uterus attachment during implantation requires ovarian estrogen in humans.…”

Section: Maternal Hormonal Environment Required For Embryo Implantsupporting

confidence: 69%

Physiological and molecular determinants of embryo implantation

Zhang

Lin

Kong

et al. 2013

Molecular Aspects of Medicine

441

480

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Embryo implantation involves the intimate interaction between an implantation-competent blastocyst and a receptive uterus, which occurs in a limited time period known as the window of implantation. Emerging evidence shows that defects originating during embryo implantation induce ripple effects with adverse consequences on later gestation events, highlighting the significance of this event for pregnancy success. Although a multitude of cellular events and molecular pathways involved in embryo-uterine crosstalk during implantation have been identified through gene expression studies and genetically engineered mouse models, a comprehensive understanding of the nature of embryo implantation is still missing. This review focuses on recent progress with particular attention to physiological and molecular determinants of blastocyst activation, uterine receptivity, blastocyst attachment and uterine decidualization. A better understanding of underlying mechanisms governing embryo implantation should generate new strategies to rectify implantation failure and improve pregnancy rates in women.

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Section: Maternal Hormonal Environment Required For Embryo Implantsupporting

confidence: 69%

Physiological and molecular determinants of embryo implantation

Zhang

Lin

Kong

et al. 2013

Molecular Aspects of Medicine

441

480

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show abstract

“…The identification of this embryonic factor(s) remains a challenging question. There is evidence that the embryo of certain species including hamsters have the capacity to produce estrogen (Perry et al 1973, Dickmann et al 1976, George & Wilson 1978, Heap et al 1981, Hoversland et al 1982, Sholl et al 1983. We have preliminary evidence that hamster preimplantation embryos express the aromatase protein (unpublished observation).…”

Section: Discussionmentioning

confidence: 59%

Leukemia inhibitory factor ligand-receptor signaling is important for uterine receptivity and implantation in golden hamsters (Mesocricetus auratus)

Ding¹,

Song²,

Wang³

et al. 2007

Reproduction

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Blastocyst implantation occurs in the progesterone-primed uterus of hamsters, but not in mice where the progesterone-primed uterus requires estrogen influence. Leukemia inhibitory factor (Lif), an estrogen-regulated gene in mice, is an absolutely needed cytokine for uterine receptivity and implantation in this species. This study aimed to evaluate the importance of Lif ligand-receptor signaling during uterine receptivity and implantation in hamsters. We investigated whether or not the uterine expression patterns of Lif and its receptors, Lif-r and gp130, during the periimplantation period of pregnancy and its hormonal regulation in the ovariectomized hamster correlate with some of the vital phases of uterine changes during early pregnancy. Uterine Lif, Lif-r, and gp130 mRNA expressions were examined by Northern and in situ hybridization. During the uterine preparatory phase for implantation, Lif, Lif-r, and gp130 were expressed either in the gland, luminal epithelium or both. As the implantation process began, Lif expression was minimal, but Lif-r and gp130 extended to the decidual areas. This decidual expression of Lif-r and gp130 was not dependent on the presence of the embryo since these genes were expressed in the sutureinduced deciduomata. We also observed that, while the uterine Lif was induced by estrogen, Lif-r and gp130 were induced by progesterone in ovariectomized hamsters. Additionally, we show that a Lif antibody when instilled intraluminally on day 3 of pregnancy reduced the number of implantation sites. Taken together, these data suggest that Lif signaling is important for uterine receptivity and implantation in hamsters. Reproduction (2008) 135 41-53

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“…Maternal recognition of pregnancy involves biochemical communication between the conceptus and its mother to provide uninterrupted synthesis and release of progesterone. Extension of luteal function beyond the length of a normal estrous cycle is the first evidence that maternal recognition of pregnancy has occurred (153,331). Although the mechanisms by which progesterone synthesis is maintained vary between species, only a few general types of signals are used, and timing of the signal is critical.…”

Section: A General Considerationsmentioning

confidence: 99%

Mechanisms Controlling the Function and Life Span of the Corpus Luteum

Niswender

Juengel

Silva

et al. 2000

Physiological Reviews

857

553

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The primary function of the corpus luteum is secretion of the hormone progesterone, which is required for maintenance of normal pregnancy in mammals. The corpus luteum develops from residual follicular granulosal and thecal cells after ovulation. Luteinizing hormone (LH) from the anterior pituitary is important for normal development and function of the corpus luteum in most mammals, although growth hormone, prolactin, and estradiol also play a role in several species. The mature corpus luteum is composed of at least two steroidogenic cell types based on morphological and biochemical criteria and on the follicular source of origin. Small luteal cells appear to be of thecal cell origin and respond to LH with increased secretion of progesterone. LH directly stimulates the secretion of progesterone from small luteal cells via activation of the protein kinase A second messenger pathway. Large luteal cells are of granulosal cell origin and contain receptors for PGF(2alpha) and appear to mediate the luteolytic actions of this hormone. If pregnancy does not occur, the corpus luteum must regress to allow follicular growth and ovulation and the reproductive cycle begins again. Luteal regression is initiated by PGF(2alpha) of uterine origin in most subprimate species. The role played by PGF(2alpha) in primates remains controversial. In primates, if PGF(2alpha) plays a role in luteolysis, it appears to be of ovarian origin. The antisteroidogenic effects of PGF(2alpha) appear to be mediated by the protein kinase C second messenger pathway, whereas loss of luteal cells appears to follow an influx of calcium, activation of endonucleases, and an apoptotic form of cell death. If the female becomes pregnant, continued secretion of progesterone from the corpus luteum is required to provide an appropriate uterine environment for maintenance of pregnancy. The mechanisms whereby the pregnant uterus signals the corpus luteum that a conceptus is present varies from secretion of a chorionic gonadotropin (primates and equids), to secretion of an antiluteolytic factor (domestic ruminants), and to a neuroendocrine reflex arc that modifies the secretory patterns of hormones from the anterior pituitary (most rodents).

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Estrogen synthesis and metabolism in the hamster blastocyst, uterus and liver near the time of implantation

Cited by 25 publications

References 24 publications

Physiological and molecular determinants of embryo implantation

Physiological and molecular determinants of embryo implantation

Leukemia inhibitory factor ligand-receptor signaling is important for uterine receptivity and implantation in golden hamsters (Mesocricetus auratus)

Mechanisms Controlling the Function and Life Span of the Corpus Luteum

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