A molecular basis for embryo apposition at the luminal epithelium

Yoon, So Ra

doi:10.1016/s0303-7207(04)00008-5

Cited by 13 publications

(19 citation statements)

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“…One reason could be that microarray-based approaches to identify genes in the uterus during the postimplantation period have focused on early implantation stages (between days 4 and 6 of pregnancy), with no separate analysis of implantation and interimplantation sites in the study by Yoshioka et al (57), for example, or with a separate study of both uterus regions but including the embryonic genomic changes as well (41). When both uterine regions have been considered, only the epithelium was studied (56). Furthermore, those early studies used Affymetrix murine U74A or Digital Genomics Mouse 6K gene chips, where the expression of no more than 7,000 genes was considered.…”

Section: Discussionmentioning

confidence: 99%

Cystathionine β-synthase deficiency causes infertility by impairing decidualization and gene expression networks in uterus implantation sites

Nuño-Ayala

Guillén

Arnal

et al. 2012

Physiological Genomics

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mocysteinemia has been reported in human reproduction as a risk factor for early pregnancy loss, preeclampsia, and congenital birth defects like spina bifida. Female infertility was also observed in cystathionine beta synthase-deficient mice (Cbs-KO) as an animal model for severe hyperhomocysteinemia. The aim for the present research was to elucidate the time-point of pregnancy loss and to pinpoint gene and cellular changes involved in the underlying pathological mechanism. By mating 90-dayold wild-type and Cbs-KO female mice with their homologous male partners, we found that pregnancy loss in Cbs-KO occurred between the 8th and 12th gestation day during placenta formation. DNA microarrays were carried out on uterus from implantation and interimplantation samples obtained on day 8. The results allowed us to select genes potentially involved in embryo death; these were individually confirmed by RT-qPCR, and their expressions were also followed throughout pregnancy. We found that changes in expression of Calb1, Ttr, Expi, Inmt, Spink3, Rpgrip1, Krt15, Gzmc, Gzmb, Tdo2, and Afp were important for pregnancy success, since a different regulation in Cbs-KO mice was found. Also, differences in relationships among selected genes were observed, indicating a dysregulation of these genes in Cbs-KO females. In conclusion, our data provide more information on the gene expression cascade and its timely regulated process required for a successful pregnancy. In addition, we unveil new potential avenues to explore further investigations in pregnancy loss.reproduction; hyperhomocysteinemia; uterus IN EPIDEMIOLOGICAL AND META-ANALYSIS studies, hyperhomocysteinemia (Hhcy) has been found to be a risk factor for placentally mediated diseases, such as preeclampsia, spontaneous abortion, and placental abruption (50). In case-control studies, it has been also reported that homocysteine (Hcy) levels are frequently elevated in complicated pregnancies due to preeclampsia or umbilical placental vascular disease over those present in the normal pregnancy group (11,37,54).Hcy is a nonprotein sulfur amino acid and a substrate for cystathionine ␤-synthase (Cbs) in the transsulfuration pathway, which represents its main metabolic fate. Alternatively, Hcy can be converted into methionine through the remethylation pathway. Three metabolic reactions using different methyl donors are known; one uses betaine, and the reaction is catalyzed by betaine-homocysteine methyltransferase, the second one catalyzed by 5-methyltetrahydrofolate-homocysteine methyltransferase uses as donor 5-methyltetrahydrofolate (43), and the third one is catalyzed by S-methylmethionine-homocysteine methyltransferase with methyl donor S-methylmethionine (46). These metabolic pathways are expressed in different tissues during development. Thus, Cbs is expressed in liver, pregnant myometrium, and decidual tissue, whereas methionine synthase is expressed in all embryonic tissues, the liver being the primary site of activity for these enzymes (48,51,58).Cbs-deficient [Cbs knockout...

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Section: Discussionmentioning

confidence: 99%

Cystathionine β-synthase deficiency causes infertility by impairing decidualization and gene expression networks in uterus implantation sites

Nuño-Ayala

Guillén

Arnal

et al. 2012

Physiological Genomics

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“…For example, in breast cancer cells IGF1R activation upregulates fascin-1, a modulator of adhesion and cell-cell interactions (Wong et al, 1999) to promote reorganization of cell-cell contacts (Guvakova et al, 2002a;Guvakova et al, 2002b;Yamashiro et al, 1998). Increased expression of fascin has been reported at implantation sites in mice, suggesting that it has a potential role in the initial adhesion stages (Yoon et al, 2004). However, in recent years it has emerged that binding and crosstalk between IGF1R and cell-cell or cell-matrix adhesion molecules can occur in either the presence or absence of IGF ligand, including with integrin avb3 Xi et al, 2008), which is involved in implantation (Kang et al, 2014;Lessey, 1997).…”

Section: Research Articlementioning

confidence: 99%

miR-145 suppresses embryo-epithelial juxtacrine communication at implantation by modulating maternal IGF1R

Kang

Lees

Matthews

et al. 2015

Journal of Cell Science

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Successful implantation requires the synchronization of viable embryonic development with endometrial receptivity. The mechanisms allowing for the initiation of crosstalk between the embryo and the endometrium remain elusive; however, recent studies have revealed that there are alterations in endometrial microRNAs (miRs) in women suffering repeated implantation failure and that one of the altered miRs is miR-145. We assessed the role of miR-145 and its target IGF1R, in early implantation. miR-145 overexpression and IGF1R knockdown were achieved in Ishikawa endometrial cells. Quantitative PCR, western blotting and 39UTR luciferase reporter assays confirmed that IGF1R is a direct target of miR-145 in the endometrium. Attachment of mouse embryos or IGF1-coated beads to endometrial epithelial cells was used to study the effects of altered miR-145 and/or IGF1R expression on early implantation events. miR-145 overexpression or specific reduction of IGF1R impaired attachment in both cases. An IGF1R target protector prevented the miR-145-mediated reduction in IGF1R and reversed the effect of miR-145 overexpression on attachment. The data demonstrate that miR-145 influences embryo attachment by reducing the level of IGF1R in endometrium.

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“…The murine studies have used several different paradigms to identify receptivity genes. These include comparisons of: implantation vs intersite tissue (whole uterus (Nie et al 2000b) or luminal epithelium only (Yoon et al 2004)), prereceptive vs receptive uterus (Yoshioka et al 2000) and delayed vs nidatory oestrogen-treated uteri (Reese et al 2001). The ability of microarrays to analyse thousands of mRNAs simultaneously provides a powerful new approach to the identification of markers of receptivity.…”

Section: The Use Of Arrays To Identify Genes Involved In Endometrial mentioning

confidence: 99%

“…In order to understand the responses of individual endometrial compartments, and how they may influence each other, it will be necessary to isolate individual cell types to determine their unique transcriptome. One solution to this problem is the technique of LCM, which has recently been used to study luminal gene changes induced by blastocyst apposition (Yoon et al 2004). In this approach, individual cells or groups of cells such as luminal or glandular epithelium can be isolated under the microscope from tissue sections and RNA from them interrogated by microarrays.…”

Section: Microarray Studies Of Endometriummentioning

confidence: 99%

Large-scale gene expression studies of the endometrium: what have we learnt?

Sherwin¹,

Catalano²,

Sharkey³

2006

Reproduction

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The endometrium is a dynamic tissue that undergoes coordinated changes under the influence of steroid hormones. This results in proliferation and differentiation culminating in a receptive state, followed by menstruation and endometrial repair. These functions involve complex interactions between the epithelium, stroma and leucocytes in the endometrium. Understanding the underlying causes of endometrial disorders, such as infertility, endometriosis and heavy menstrual bleeding, therefore represents a considerable challenge. Recently developed techniques, such as differential display and DNA microarrays permit the abundance of thousands of mRNA transcripts within cells or tissues to be measured simultaneously. This provides a new approach to understanding the complex interactions that underlie both healthy and disease states. Responses of the endometrium to hormones or drugs can be studied and the response of the system as an integrated whole can be assessed. Comparisons of endometrium from healthy women and those with endometrial dysfunction have advanced our understanding of key areas of endometrial physiology, including infertility, receptivity, endometriosis and cancer. Using this approach, novel genes controlling specific endometrial functions like receptivity have been identified for functional testing. This paper will review the impact of these techniques for transcript profiling on our understanding of selected areas of endometrial biology and discuss the potential applications in future.

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A molecular basis for embryo apposition at the luminal epithelium

Cited by 13 publications

References 0 publications

Cystathionine β-synthase deficiency causes infertility by impairing decidualization and gene expression networks in uterus implantation sites

Cystathionine β-synthase deficiency causes infertility by impairing decidualization and gene expression networks in uterus implantation sites

miR-145 suppresses embryo-epithelial juxtacrine communication at implantation by modulating maternal IGF1R

Large-scale gene expression studies of the endometrium: what have we learnt?

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