Comparative analysis of mouse decidualization models by using RNA-seq
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE122376 | GEO | 2018/11/10
REPOSITORIES: GEO
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Project description:The zinc-finger transcription factor GATA2 has been shown to be important for endometrial stromal cell decidualization in early pregnancy in mice and humans. Progesterone and its receptor PGR is also critical during decidualization but its interaction with GATA2 in regulating genes and pathways necessary for decidualization in human endometrium are unclear. Human endometrial stromal cells were isolated from 5 premenopausal women for primary cell culture. The cells underwent in vitro decidualization (IVD) or vehicle (Veh) treatment for 10 days. RNA-sequencing (RNA-seq) was performed to compare gene expression profiles (n=3) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) using an antibody against GATA2 (n=2) was performed to examine binding to target genes in the Veh and IVD cells. A public PGR ChIP-seq dataset (GSE69539) was mined to identify PGR-binding regions in IVD-treated human endometrial cells.
2020-02-22 | GSE145673 | GEO
Project description:The zinc-finger transcription factor GATA2 has been shown to be important for endometrial stromal cell decidualization in early pregnancy in mice and humans. Progesterone and its receptor PGR is also critical during decidualization but its interaction with GATA2 in regulating genes and pathways necessary for decidualization in human endometrium are unclear. Human endometrial stromal cells were isolated from 5 premenopausal women for primary cell culture. The cells underwent in vitro decidualization (IVD) or vehicle (Veh) treatment for 10 days. RNA-sequencing (RNA-seq) was performed to compare gene expression profiles (n=3) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) using an antibody against GATA2 (n=2) was performed to examine binding to target genes in the Veh and IVD cells. A public PGR ChIP-seq dataset (GSE69539) was mined to identify PGR-binding regions in IVD-treated human endometrial cells.
2020-02-22 | GSE145671 | GEO
Project description:Uterine glands and, by inference, their secretions impact uterine receptivity, blastocyst implantation, stromal cell decidualization, and placental development. Changes in gland function across the menstrual cycle are impacted by steroid hormones, estrogen and progesterone, as well as stroma-derived factors. Using an endometrial epithelial organoid (EEO) system, transcriptome and proteome analyses identified distinct responses of the EEO to steroid hormones and prostaglandin E2 (PGE2). Notably, steroid hormones and PGE2 modulated the basolateral secretion of EEO proteins, where cystatin C (CST3) was significantly increased by progesterone and PGE2. CST3 treatment of decidualizing stromal cells significantly decreased the decidualization markers PRL and IGFBP1. The attenuation of stromal cell decidualization via CST3 suggests a role for uterine gland-derived proteins in controlling the extent of decidualization. These findings provide evidence that uterine gland-derived factors directly impact stromal cell decidualization, which has strong implications for better understanding pregnancy establishment and female fertility in humans.
2023-10-11 | PXD034357 | Pride
Project description:Uterine receptivity implies a dialogue between the hormonally primed maternal endometrium and the free-floating blastocyst. Endometrial stromal cells proliferate, avert apoptosis, and undergo decidualization in preparation for implantation; however, the molecular mechanisms that underlie differentiation into the decidual phenotype remain largely undefined. The Notch family of transmembrane receptors transduce extracellular signals responsible for cell survival, cell-to-cell communication, and trans-differentiation, all fundamental processes for decidualization and pregnancy. Using a murine artificial decidualization model, pharmacological inhibition of Notch signaling by gamma-secretase inhibition resulted in significantly decreased deciduoma. Furthermore, a progesterone receptor (PR)-Cre Notch1 bigenic (Notch1d/d) confirmed a Notch1-dependant hypomorphic decidual phenotype. Microarray and pathway analysis, following Notch1 ablation, demonstrated significantly altered signaling repertoire. Concomitantly, hierarchical clustering demonstrated Notch1-dependent differences in gene expression. Uteri deprived of Notch1 signaling demonstrated decreased cellular proliferation; namely, reduced proliferation-specific antigen, Ki67, altered p21, cdk6, and cyclinD activity, and increased apoptotic-profile, augmented cleaved caspase-3, Bad, and attenuated Bcl2. Demonstrated here, the pre-implantation uterus relies on Notch signaling to inhibit apoptosis of stromal fibroblasts and regulate cell cycle progression, which together promotes successful decidualization. In summary, Notch1 signaling modulates multiple signaling mechanisms crucial for decidualization and we provide greater perspective to the coordination of multiple signaling modalities required during decidualization RNA samples from 3-5 separate mice were extracted. All mRNA quantities were normalized against 18S gene expression. Gene expression levels were measured by real-time RT-PCR SYBR Green analysis using the ABI Prism 7700 Sequence Detector System according to manufacturer’s instructions (Applied Biosystems).
2011-08-08 | E-GEOD-31244 | biostudies-arrayexpress
Project description:Analysis of differences in gene expression in the mouse uterus during decidualization in the presence and absence of a conceptus. A deciduomal model previously shown to better mimick natural decidualization was used. The results reveal some, but very few, genes that are differentially expressed, which is unlike previous reports using other deciduomal models shown previously to not mimick natural decidualization. Total RNA obtained from isolated uterine segment tissue undergoing decidualization from pregnant or pseudopregnant mice. Three replicates per condition.
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Project description:Uterine receptivity implies a dialogue between the hormonally primed maternal endometrium and the free-floating blastocyst. Endometrial stromal cells proliferate, avert apoptosis, and undergo decidualization in preparation for implantation; however, the molecular mechanisms that underlie differentiation into the decidual phenotype remain largely undefined. The Notch family of transmembrane receptors transduce extracellular signals responsible for cell survival, cell-to-cell communication, and trans-differentiation, all fundamental processes for decidualization and pregnancy. Using a murine artificial decidualization model, pharmacological inhibition of Notch signaling by gamma-secretase inhibition resulted in significantly decreased deciduoma. Furthermore, a progesterone receptor (PR)-Cre Notch1 bigenic (Notch1d/d) confirmed a Notch1-dependant hypomorphic decidual phenotype. Microarray and pathway analysis, following Notch1 ablation, demonstrated significantly altered signaling repertoire. Concomitantly, hierarchical clustering demonstrated Notch1-dependent differences in gene expression. Uteri deprived of Notch1 signaling demonstrated decreased cellular proliferation; namely, reduced proliferation-specific antigen, Ki67, altered p21, cdk6, and cyclinD activity, and increased apoptotic-profile, augmented cleaved caspase-3, Bad, and attenuated Bcl2. Demonstrated here, the pre-implantation uterus relies on Notch signaling to inhibit apoptosis of stromal fibroblasts and regulate cell cycle progression, which together promotes successful decidualization. In summary, Notch1 signaling modulates multiple signaling mechanisms crucial for decidualization and we provide greater perspective to the coordination of multiple signaling modalities required during decidualization
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Project description:Proper decidualization is a critical determinant of pregnancy success. Deficiencies in decidualization are associated with a variety of pregnancy disorders, including female infertility, recurrent implantation failure, and miscarriage. However, the mechanism for triggering decidualization of human endometrium is largely unknown. Here we characterized the transcriptomes of four major cells in human endometrium and decidua at single-cell resolution. We discovered the dynamic change characteristics of six major stromal cells. More importantly, a dialogue between IGF1+ stromal cells and IGF1R+ stromal cells initiates endometrial decidualization under regulation of progesterone and estrogen, and IL1B+ stromal cells trigger the apoptosis of epithelial cells and functional remodeling during decidualization. We defined a unique AREG+ NK cell for accelerating decidualization by interacting with IGF1+ stromal cells, and observed that extravillous trophoblasts promote decidualization possibly by multiply pathways. Additionally, we developed a systematic repository of cell-cell communication for decidualization via the ligand-receptor complexes interactions. Our study provides deeper insights into the molecular and cellular characterizations during decidualization.
2022-11-24 | GSE194219 | GEO
Project description:Analysis of differences in gene expression in the mouse uterus during decidualization in the presence and absence of a conceptus. A deciduomal model previously shown to better mimick natural decidualization was used. The results reveal some, but very few, genes that are differentially expressed, which is unlike previous reports using other deciduomal models shown previously to not mimick natural decidualization.
2011-11-20 | GSE25903 | GEO
Project description:Uterine glands and, by inference, their secretions impact uterine receptivity, blastocyst implantation, stromal cell decidualization, and placental development. Changes in gland function across the menstrual cycle are impacted by steroid hormones, estrogen and progesterone, as well as stroma-derived factors. Using an endometrial epithelial organoid (EEO) system, transcriptome and proteome analyses identified distinct responses of the EEO to steroid hormones and prostaglandin E2 (PGE2). Notably, steroid hormones and PGE2 modulated the basolateral secretion of EEO proteins, where cystatin C (CST3) was significantly increased by progesterone and PGE2. CST3 treatment of decidualizing stromal cells significantly decreased the decidualization markers PRL and IGFBP1. The attenuation of stromal cell decidualization via CST3 suggests a role for uterine gland-derived proteins in controlling the extent of decidualization. These findings provide evidence that uterine gland-derived factors directly impact stromal cell decidualization, which has strong implications for better understanding pregnancy establishment and female fertility in humans.
2022-06-06 | GSE205084 | GEO
Project description:In the present study, we aimed to discern the preconception decidual transcriptomic signature associated with in vivo defective decidualization in women who suffered sPE in a previous pregnancy. First, we performed a comparative global transcriptional profiling of endometrium from women who developed sPE in a previous pregnancy and from women who never have had sPE. Then, we selected those genes that were significantly deregulated 1.4-fold higher (FDR<0.05) and have an EntrezID code. As a result, we formulate a transcriptional signature associated with defective decidualization composed by 120 genes.
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