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Differential expression of Wnt signalling molecules between pre- and post-menopausal endometrial epithelial cells suggests that a population of putative epithelial stem/progenitor cells reside in the basalis layer

ABSTRACT: The human endometrium is a highly regenerative tissue that undergoes cyclical proliferation, differentiation and shedding each month. The upper functionalis layer of the endometrium is shed in response to circulating levels of estrogen and progesterone, while the lower basalis layer remains. Clonogenic epithelial stem/progenitor cells likely responsible for regenerating endometrial epithelium have been identified in pre-menopausal (Pre-M) and post-menopausal (Post-M) endometrium and may reside in the basalis layer. We undertook a transcriptional profiling of purified epithelial cells from full-thickness Pre-M and Post-M endometrium to identify differentially expressed genes. The hypothesis tested in the present study was that Post-M endometrial epithelial gene profile would be similar to the quiescent basalis epithelium of Pre-M endometrium. We found striking differential gene expression of many Wnt family members between Pre-M and Post-M and other stem cell network genes. Comparative analysis of our endometrial epithelial gene expression profiles to that of endometrial epithelial cells in remodelling endometrium also provides new evidence showing that Post-M endometrial epithelium has a similar gene signature to that of basalis epithelium of menstrual endometrium.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35221 | GEO | 2012/04/11

SECONDARY ACCESSION(S): PRJNA150653

REPOSITORIES: GEO

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Differential expression of Wnt signalling molecules between pre- and post-menopausal endometrial epithelial cells suggests that a population of putative epithelial stem/progenitor cells reside in the basalis layer

Project description:The human endometrium is a highly regenerative tissue that undergoes cyclical proliferation, differentiation and shedding each month. The upper functionalis layer of the endometrium is shed in response to circulating levels of estrogen and progesterone, while the lower basalis layer remains. Clonogenic epithelial stem/progenitor cells likely responsible for regenerating endometrial epithelium have been identified in pre-menopausal (Pre-M) and post-menopausal (Post-M) endometrium and may reside in the basalis layer. We undertook a transcriptional profiling of purified epithelial cells from full-thickness Pre-M and Post-M endometrium to identify differentially expressed genes. The hypothesis tested in the present study was that Post-M endometrial epithelial gene profile would be similar to the quiescent basalis epithelium of Pre-M endometrium. We found striking differential gene expression of many Wnt family members between Pre-M and Post-M and other stem cell network genes. Comparative analysis of our endometrial epithelial gene expression profiles to that of endometrial epithelial cells in remodelling endometrium also provides new evidence showing that Post-M endometrial epithelium has a similar gene signature to that of basalis epithelium of menstrual endometrium. Human endometrial tissue was obtained from 8 pre-menopausal and 3 post-menopausal women undergoing hysterectomy for various benign gynaecologic conditions. Endometrial tissue was digested and isolated using combination of DNase and collagenase. Anti-human EpCAM antibody-coated magnetic Dynabeads was used to positively select total epithelial cells from the digested single cell suspensions. Total RNA was extracted from the purified endometrial epithelial cells and hybridised to Illumina Sentrix HT12 beadchip. Resulting data was compared between pre-menopausal and post-menopausal samples.

2012-04-10 | E-GEOD-35221 | biostudies-arrayexpress

Homo sapiens

Project description:Differential expression of Wnt signalling molecules between pre- and post-menopausal endometrial epithelial cells suggests that a population of putative epithelial stem/progenitor cells reside in the basalis layer

| PRJNA150653 | ENA

SECRETORY PROTEOMIC RESPONSES OF ENDOMETRIAL EPITHELIAL CELLS TO TROPHOBLAST DERIVED EXTRACELLULAR VESICLES

Project description:Synchronized cross talk between embryo and endometrium during pre-implantation period is critical for establishment of pregnancy. Extracellular vesicels(EVs) of both embryo and endometrial origin are known to be integral in regulating embryo maternal communication during this time. However, exact molecular signalling pathways or factors that regulate the embryo endometrial communication during pre-conception period remains elusive. Here in this study extracellular vesicles from trophoblast cells were shown to modulate endometrial epithelial cell secretome in favour of embryo implantation and embryo development.

2023-10-24 | PXD040311 | Pride

Endometrial epithelial Arid1a is essential in early pregnancy

Project description:Endometrial epithelial Arid1a is necessary for normal gene expression and maintenance of a receptive endometrium at pre-implantation stage in mice. We used RNA-sequencing to determine the differences in uterine gene expression resulting from deletion of endometrial epithelial Arid1a.

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Adiposity alters protective mechanisms of progesterone through dysregulation of endometrial metallothionein expression

Project description:In this study, we sought to understand the effects of excess adipose on the benign endometrium. We used a physiologic in vitro coculture system consisting of multicellular organoids of the benign human endometrium and adipose spheroids in the presence of estradiol, progesterone, and testosterone to mimic the menstrual cycle. Gene expression analysis of endometrial organoids under high adiposity conditions revealed downregulation of genes normally expressed in secretory endometrium, suggestive of an altered progesterone response. Genes associated with ion homeostasis and detoxification of reactive oxygen species were also downregulated, including the metallothionein (MT) family of genes. We demonstrated that MT gene expression in endometrial organoids was regulated by progesterone specifically in the epithelial cells, and that progesterone receptor is recruited to the promoters of MT genes in endometrial epithelial cells. We illustrated the impact of MT dysregulation by silencing MT genes in endometrial epithelial cells, resulting in increased DNA damage. Our results reveal that exposing the endometrium to high adiposity can compromise the protective effects of progesterone, dysregulate MT genes in the endometrial epithelium, and leave the endometrium vulnerable to ROS-induced DNA damage.

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Effects of long-term treatment with tamoxifen on endometrial gene expression in women.

Project description:The aim was to examine changes in gene expression of the endometrium exposed to long-term tamoxifen treatment in comparison to age matched controls. To achieve this, endometrial tissues were obtained from women receiving tamoxifen treatment who were undergoing a hysterectomy. Using cDNA microarrays, gene expression changes in the postmenopausal endometrium of these women was compared with that in endometrium of age matched women not receiving tamoxifen. Endometrial tissue from post-menopausal women was obtained following ethical approval from the Leicester NHS Trust. None of the women had received any hormonal treatment for two months prior to the procurement of the specimens. Tissues were taken from untreated women (n=6) or those treated for 4 to 5 years with tamoxifen (20mg/day) (n=4), aged 58-82 (65 Â± 9.1, mean Â± SD). Total RNA was extracted. Controls were pooled. RNA labelling, hybridisation and analysis of fluorescence was carried out as described by Turton et al (2001). Cy3/Cy5 Dye swap labelling was carried out on samples from each patient. Reference: Turton NJ et. al. (Oncogene (2001) 20, 1300-1306

2010-06-30 | E-GEOD-3626 | biostudies-arrayexpress

Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis [CUT&RUN]

Project description:TP53 and ARID1A are frequently mutated across cancer but rarely in the same primary tumor. Endometrial cancer has the highest TP53-ARID1A mutual exclusivity rate. However, the functional relationship between TP53 and ARID1A mutations in the endometrium has not been elucidated. We used genetically engineered mice and in vivo genomic approaches to discern both unique and overlapping roles of TP53 and ARID1A in the endometrium. TP53 loss with oncogenic PIK3CA*H1047R in the endometrial epithelium results in features of endometrial hyperplasia, adenocarcinoma, and intraepithelial carcinoma. Mutant endometrial epithelial cells were transcriptome profiled and compared to control cells and ARID1A/PIK3CA mutant endometrium. In the context of either TP53 or ARID1A loss, PIK3CA mutant endometrium exhibited inflammatory pathway activation, but other gene expression programs differed based on TP53 or ARID1A status, such as epithelial-to-mesenchymal transition. Gene expression patterns observed in the genetic mouse models are reflective of human tumors with each respective genetic alteration. Consistent with TP53-ARID1A mutual exclusivity, the p53 pathway is activated following ARID1A loss in the endometrial epithelium, where ARID1A normally directly represses p53 pathway genes in vivo, including the stress-inducible transcription factor, ATF3. However, co-existing TP53-ARID1A mutations led to invasive adenocarcinoma associated with mutant ARID1A-driven ATF3 induction, reduced apoptosis, TP63+ squamous differentiation and invasion. These data suggest TP53 and ARID1A mutations drive shared and distinct tumorigenic programs in the endometrium and promote invasive endometrial cancer when existing simultaneously. Hence, TP53 and ARID1A mutations may co-occur in a subset of aggressive or metastatic endometrial cancers, with ARID1A loss promoting squamous differentiation and the acquisition of invasive properties.

2021-12-13 | GSE184498 | GEO

Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis [RNA-seq]

2021-12-13 | GSE167275 | GEO

The analysis of the α2,6-sialylated proteins in endometrium from porcine gestational day 15 by LC-MS/MS

Project description:Implantation is the attachment of embryo in the endometrium. Failure in implantation is a major cause of early pregnancy loss. During implantation, the temporal uterine lumen closure can help embryo attach to the uterus. In pigs, extending of endometrial folds to form interlocking finger-like projections is a main cause leads to uterine lumen closure during attachment time, but the underlying mechanisms are largely unknown. Our data reveal that pig uterine luminal epithelium (LE) migrate in coordinated groups during extending of endometrial folds. Moreover, the MALDI-TOF MS based N-glycomic characterization of porcine endometrium revealed α2,6-linked sialic acid are highly expressed in pig uterine LE during extending of endometrial folds. To investigated the mechanisms by which α2,6-sialylated proteins in formation of the endometrial folding during implantation in pigs, the α2,6-sialylated proteins in pig uterine LE were characterized by proteomic analysis and those proteins that are involved in cell adhesion, such as E-cadherin, were detected. Finally, our in vivo and in vitro data show that α2,6-sialylation of E-cadherin occurs in accompany with collective epithelial migration. The results provide new insight into the mechanism of pig implantation by identifying that α2,6-sialylation of cell adhesion molecules may participate in formation of extending of endometrial folds through promoting of collective migration of uterine LE.

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Epigenetic regulation of receptive human endometrium through microRNAs

Project description:MicroRNAs (miRNAs) act as important epigenetic post-transcriptional regulators of gene expression. We aimed to gain more understanding to the complex gene expression regulation of endometrial receptivity by analysing miRNA signature of fertile human endometrium. We used Agilent miRNA arrays to define the miRNA expression pattern in receptive (LH+7, n = 3) vs. pre-receptive (LH<7, n = 4) endometrium from healthy fertile women.

2012-06-22 | E-GEOD-34435 | biostudies-arrayexpress

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