Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-62854
PROVIDER: PRJNA265850 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1635334.fastq.gz | Fastqsanger.gz | |||
| SRR1635335.fastq.gz | Fastqsanger.gz | |||
| SRR1635336.fastq.gz | Fastqsanger.gz | |||
| SRR1635337.fastq.gz | Fastqsanger.gz | |||
| SRR1635338.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Implantation is dependent on synchronized interactions between the conceptus and surrounding decidual cells but the involvement of clock genes in this process is not well understood. Circadian oscillations are predicated on transcriptional-translational feedback loops, which balance the activities of the transcriptional activators CLOCK and BMAL1 and repressors encoded by PER and CRY genes. Here we show that loss of PER2 expression silences circadian oscillations in decidualizing human endometrial stromal cells (HESCs). Downregulation was preceded by reduced CLOCK binding to a noncanonical E-box enhancer in the PER2 promoter and occurred between 12 - 24 h after exposure to a deciduogenic stimulus. RNA sequencing revealed that premature inhibition of PER2 by siRNA knockdown leads to a grossly disorganised decidual response. Gene ontology analysis highlighted a preponderance of cell cycle regulators amongst the 1,121 genes perturbed upon PER2 knockdown. Congruently, PER2 inhibition abrogated mitotic expansion of differentiating HESCs by inducing cell cycle block at G2/M. Analysis of mid-luteal endometrial biopsies revealed an inverse correlation between PER2 transcript levels and the number of miscarriages in women suffering reproductive failure. Thus, PER2 synchronizes mitotic expansion of HESCs with a periodic decidual gene expression; uncoupling of these events may cause persistent pregnancy failure. Endometrial mRNA profiles of paired control (siRNA-NT) and siRNA-PER2 were generated by deep sequencing, in triplicate using Illumina
2015-09-16 | E-GEOD-62854 | biostudies-arrayexpress
Project description:Implantation is dependent on synchronized interactions between the conceptus and surrounding decidual cells but the involvement of clock genes in this process is not well understood. Circadian oscillations are predicated on transcriptional-translational feedback loops, which balance the activities of the transcriptional activators CLOCK and BMAL1 and repressors encoded by PER and CRY genes. Here we show that loss of PER2 expression silences circadian oscillations in decidualizing human endometrial stromal cells (HESCs). Downregulation was preceded by reduced CLOCK binding to a noncanonical E-box enhancer in the PER2 promoter and occurred between 12 - 24 h after exposure to a deciduogenic stimulus. RNA sequencing revealed that premature inhibition of PER2 by siRNA knockdown leads to a grossly disorganised decidual response. Gene ontology analysis highlighted a preponderance of cell cycle regulators amongst the 1,121 genes perturbed upon PER2 knockdown. Congruently, PER2 inhibition abrogated mitotic expansion of differentiating HESCs by inducing cell cycle block at G2/M. Analysis of mid-luteal endometrial biopsies revealed an inverse correlation between PER2 transcript levels and the number of miscarriages in women suffering reproductive failure. Thus, PER2 synchronizes mitotic expansion of HESCs with a periodic decidual gene expression; uncoupling of these events may cause persistent pregnancy failure.
2015-09-16 | GSE62854 | GEO
Project description:The fate of the human endometrium is determined during the mid-luteal window of implantation, coinciding with differentiation of endometrial stromal cells (EnSCs) into specialized decidual cells. Upon embryo implantation, differentiating EnSCs transform the endometrium into the decidua of pregnancy; whereas falling progesterone levels in the absence of pregnancy lead to tissue breakdown and menstruation. We used single-cell RNA sequencing to map the transcriptomic changes in primary EnSCs along a decidual time-course and in response to withdrawal of differentiation signals. We demonstrate that decidual transformation starts with a precipitous transcriptional response, which is followed by synchronous transition of EnSCs through intermediate states before emerging as divergent subpopulations, representing decidual cells and senescent decidual cells. Single-cell analysis of timed luteal phase biopsies identified multiple endometrial epithelial subpopulations and immune cells, most prominently uterine NK cells. In the stroma, transition from receptive to post-receptive endometrial state was marked by progression of EnSCs along diverging transcriptional trajectories, involving genes with conserved branching dynamics in vivo and in vitro. Our findings indicate that specification of EnSCs into distinct decidual subpopulations underpins endometrial fate decisions during the window of implantation.
2020-01-06 | GSE127918 | GEO
Project description:We sequenced mRNA from hypoxia treated endometrial stromal fibroblasts and decidual stromal cells in order to better understand endometrial hypoxia responses
2019-01-01 | GSE111570 | GEO
Project description:Decidual remodelling of midluteal endometrium leads to a short implantation window after which the uterine mucosa either breaks down or is transformed into a robust matrix that accommodates the placenta throughout pregnancy. To gain insights into the underlying mechanisms, we established and characterised endometrial assembloids, consisting of gland organoids and primary stromal cells. Single-cell transcriptomics revealed that decidualized assembloids closely resemble midluteal endometrium, harbouring differentiated and senescent subpopulations in both glands and stroma. We show that acute senescence in glandular epithelium drives secretion of multiple canonical implantation factors, whereas in the stroma it calibrates the emergence of anti-inflammatory decidual cells and pro-inflammatory senescent decidual cells. Pharmacological inhibition of stress responses in pre-decidual cells accelerated decidualization by inhibiting senescence and mesenchymal-epithelial transition, processes involved in endometrial breakdown and regeneration, respectively. Accelerated decidualization resulted in entrapment of co-cultured human blastocysts in a largely static decidual matrix. By contrast, the presence of senescent decidual cells created a dynamic implantation environment, enabling embryo expansion and attachment, although their persistence led to gradual disintegration of assembloids. Together, our findings demonstrate that senescence controls endometrial fate decisions at implantation and highlight how endometrial assembloids may accelerate the discovery of new treatments to prevent reproductive failure.
2021-03-08 | GSE168405 | GEO
Project description:The peripheral circadian oscillator plays an essential role in synchronizing local physiology to operate in a circadian manner via regulation of the expression of clock-controlled genes. In the murine uterus, the endometrial stromal cells undergo proliferation and differentiation into decidual cells in response to ovarian steroids and blastocyst implantation at the early stage of pregnancy. The circadian clock genes are attenuated in the decidualizing cells only 2 days after implantation. The present study aimed to evaluate the circadian rhythms of clock genes and clock-controlled genes expressed in the rat uterus endometrial stromal cells (UESCs) during the stage of implantation. The real-time monitoring system of Per2 promoter activity was employed to precisely evaluate the generation of circadian rhythms in the UESCs prepared from transgenic rats constructed with mouse Per2 promoter-destabilized luciferase reporter gene (Per2-dLuc). During monitoring Per2-dLuc oscillation after synchronization with dexamethasone, total RNA was isolated from the cultured UESCs at four-time points (6-h interval) in the first to second phases and cDNA was synthesized. cRNA was synthesized from the double strand cDNA and hybridized on a DNA microarray. RT-qPCR was performed to confirm the expression of core clock genes revealed by DNA microarray analysis. Several clock genes such as Bmal1, Rev-erbα, and Per2 displayed significant rhythms. Of 12,252 genes showing significantly expression, 7,235 genes displayed significant alterations (p < 0.05). These genes were related to growth factors, transcription factors, receptors, channels, and enzymes. Some candidates as clock-controlled genes were evaluated by using RNA interference to Bmal1 mRNA. Down-regulation of Igf1 gene expression was observed by Bmal1 silencing, whereas the expression of Inhβa, Fas, and Caspase3 were significantly increased. These results indicate that clock-controlled genes are up- or down-regulated in rat UESCs during the stage of decidualization. DNA microarray analysis coupled with RNA interference will be helpful to understand the physiological roles of some oscillating genes in blastocyst implantation and placenta formation. The circadian clock positively or negatively regulates the expression of clock-controlled genes, including growth factors and apoptosis-related factors. To search the clock-controlled genes expressed during the period of implantation, we analyzed the clock genes and clock-controlled genes expressed in cultured uterus endometrial stromal cells prepared from pregnant rats at the stage of implantation using DNA microarray technology. We used transgenic rats constructed with mouse Per2 promoter-destabilized luciferase (Per2-dLuc) reporter gene to precisely adjust the time of gene expression. In addition, several genes of significantly expressed genes including growth factor genes and apoptosis-related genes were analyzed using RNA interference to Bmal1 mRNA whether these were controlled under circadian clockwork.
2013-07-23 | E-GEOD-49080 | biostudies-arrayexpress
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288994 | GEO
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288883 | GEO
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288877 | GEO
Project description:The endometrial expression and activity of the transcriptional co-regulator, Zinc Finger MIZ-Type Containing 1 (Zmiz1), that is co-localized with a mouse uterine estrogen receptor α (ERα)-binding super-enhancer, has not yet been evaluated. In human endometrial biopsy samples ZMIZ1 transcript and protein is dynamically expressed during the menstrual cycle. ZMIZ1 mutations are associated with some uterine tumors and ZMIZ1 RNA levels are increased in endometrium from individuals with endometriosis. Disrupting ZMIZ1 in cultured human endometrial stromal cells or in mouse uterus prevented hormone-dependent proliferation of epithelial and stromal cells as well as decidual differentiation of stroma cells, triggering sterility. Additionally, aging-dependent fibrosis was accelerated in Zmiz1-targeted mouse uterus. Notably, ZMIZ1 deletion impacted expression of stromal cell progesterone receptor (PGR), which is essential for decidual transformation. ZMIZ1 and ERα were co-localized in nuclei of mouse uterine cells, and E2F, CCNA2 and FOXM1 signaling were all decreased when ZMIZ1 was targeted, which likely underlies reduced cell cycle progression. Transcriptomic analyses revealed that loss of ZMIZ1 alters the amplitude of estrogen regulated gene responses, indicating ZMIZ1 fine-tunes endometrial cell signals needed for optimal functioning. Our findings demonstrate the importance of ZMIZ1 as an ERα co-regulator in uterine biology and pathology.
2025-09-22 | GSE288872 | GEO