Embryo Implantation

Carson, Daniel D.; Bagchi, Indrani C.; Dey, S. K.; Enders, Allen C.; Fazleabas, Asgerally T.; Lessey, Bruce A.; Yoshinaga, Koji

doi:10.1006/dbio.2000.9767

Cited by 700 publications

(573 citation statements)

References 195 publications

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“…To examine whether alterations in expression of specific uterine genes at 6.5 dpc accompany the reduced number of implantation sites noted in Bteb1 Ϫ/Ϫ mice, uteri from WT and Bteb1 Ϫ/Ϫ mice at 6.5 dpc were evaluated by QPCR for expression of progesterone-responsive, Bteb1-regulated, and/or implantation-specific genes (37,38,44,45) (Fig. 7).…”

Section: Increased Incidence Of Neonatal Lethality For Bteb1 ϫ/ϫmentioning

confidence: 99%

Subfertility, Uterine Hypoplasia, and Partial Progesterone Resistance in Mice Lacking the Krüppel-like Factor 9/Basic Transcription Element-binding Protein-1 (Bteb1) Gene

Simmen

Eason

McQuown³

et al. 2004

Journal of Biological Chemistry

119

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Progesterone receptor (PR), a ligand-activated transcription factor, is a key regulator of cellular proliferation and differentiation in reproductive tissues. The transcriptional activity of PR is influenced by co-regulatory proteins typically expressed in a tissue-and cellspecific fashion. We previously demonstrated that basic transcription element-binding protein-1 (BTEB1), a member of the Sp/Krü ppel-like family of transcription factors, functionally interacts with the two PR isoforms, PR-A and PR-B, to mediate progestin sensitivity of target genes in endometrial epithelial cells in vitro. Here we report that ablation of the Bteb1 gene in female mice results in uterine hypoplasia, reduced litter size, and increased incidence of neonatal deaths in offspring. The reduced litter size is solely a maternal genotype effect and results from fewer numbers of implantation sites, rather than defects in ovulation. In the early pregnant uterus, Bteb1 expression in stromal cells temporally coincides with PR-A isoform-dependent decidual formation at the time of implantation. Expression of two implantation-specific genes, Hoxa10 and cyclin D3, was decreased in uteri of early pregnant Bteb1-null mutants, whereas that of Bteb3, a related family member, was increased, the latter possibly compensating for the loss of Bteb1. Progesterone responsiveness of several uterine genes was altered with Bteb1-null mutation. These results identify Bteb1 as a functionally relevant PR-interacting protein and suggest its selective modulation of cellular processes that are regulated by PR-A in the uterine stroma.

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Section: Increased Incidence Of Neonatal Lethality For Bteb1 ϫ/ϫmentioning

confidence: 99%

Subfertility, Uterine Hypoplasia, and Partial Progesterone Resistance in Mice Lacking the Krüppel-like Factor 9/Basic Transcription Element-binding Protein-1 (Bteb1) Gene

Simmen

Eason

McQuown³

et al. 2004

Journal of Biological Chemistry

119

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“…[1][2][3]. In mice and rats, estrogen is essential for preparation of the progesterone (P 4 )-primed uterus to the receptive state when the uterine milieu becomes favorable to blastocyst acceptance and implantation (1,4).…”

mentioning

confidence: 99%

Estrogen is a critical determinant that specifies the duration of the window of uterine receptivity for implantation

Song²,

Das³

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

465

334

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Many underlying causes of human infertility have been overcome by using in vitro fertilization (IVF) and embryo transfer (ET) techniques. Nevertheless, implantation rates in IVF programs remain low despite the transfer of apparently healthy embryos. This suggests that there are problems with the differentiation of the uterus to the receptive state in response to the ovarian hormones estrogen and progesterone. The molecular basis of this receptive state when the uterine environment is conducive to blastocyst acceptance and implantation remains poorly understood. Normally, the ''window'' of uterine receptivity lasts for a limited time. Using ETs and the progesterone-treated delayed-implantation model in mice, we demonstrate here that levels of estrogen within a very narrow range determine the duration of the window of uterine receptivity. Although estrogen at different physiological concentrations can initiate implantation, we find that the window of uterine receptivity remains open for an extended period at lower estrogen levels but rapidly closes at higher levels. The uterine refractoriness that follows the receptive state at high estrogen levels is accompanied by aberrant uterine expression of implantation-related genes. These results suggest that careful regulation of estrogen levels is one of the important factors for improvement of female fertility in IVF͞ET programs.

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“…Successful embryo implantation depends upon bi-directional communication between the blastocyst and the uterus. Recent advances in our ability to define complex biochemical and genetic pathways have begun to unfold the molecular mechanisms underlying the regulation of implantation (1,2). Although numerous factors involved in implantation have been identified (3)(4)(5), targeted mutations in mice have revealed only a few genes that are essential to this process (6 -11).…”

mentioning

confidence: 99%

Global Gene Expression Analysis to Identify Molecular Markers of Uterine Receptivity and Embryo Implantation

Reese¹,

Das²,

Paria³

et al. 2001

Journal of Biological Chemistry

204

152

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Infertility and spontaneous pregnancy losses are an enduring problem to women's health. The establishment of pregnancy depends on successful implantation, where a complex series of interactions occurs between the heterogeneous cell types of the uterus and blastocyst. Although a number of genes are implicated in embryo-uterine interactions during implantation, genetic evidence suggests that only a small number of them are critical to this process. To obtain a global view and identify novel pathways of implantation, we used a dual screening strategy to analyze the expression of nearly 10,000 mouse genes by microarray analysis. Comparison of implantation and interimplantation sites by a conservative statistical approach revealed 36 up-regulated genes and 27 down-regulated genes at the implantation site. We also compared the uterine gene expression profile of progesterone-treated, delayed implanting mice to that of mice in which delayed implantation was terminated by estrogen. The results show up-regulation of 128 genes and down-regulation of 101 genes after termination of the delayed implantation. A combined analysis of these experiments showed specific up-regulation of 27 genes both at the implantation site and during uterine activation, representing a broad diversity of molecular functions. In contrast, the majority of genes that were decreased in the combined analysis were related to host immunity or the immune response, suggesting the importance of these genes in regulating the uterine environment for the implanting blastocyst. Collectively, we identified genes with recognized roles in implantation, genes with potential roles in this process, and genes whose functions have yet to be defined in this event. The identification of unique genetic markers for the onset of implantation signifies that genome-wide analysis coupled with functional assays is a promising approach to resolve the molecular pathways required for successful implantation.

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Embryo Implantation

Cited by 700 publications

References 195 publications

Subfertility, Uterine Hypoplasia, and Partial Progesterone Resistance in Mice Lacking the Krüppel-like Factor 9/Basic Transcription Element-binding Protein-1 (Bteb1) Gene

Subfertility, Uterine Hypoplasia, and Partial Progesterone Resistance in Mice Lacking the Krüppel-like Factor 9/Basic Transcription Element-binding Protein-1 (Bteb1) Gene

Estrogen is a critical determinant that specifies the duration of the window of uterine receptivity for implantation

Global Gene Expression Analysis to Identify Molecular Markers of Uterine Receptivity and Embryo Implantation

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