Single cell insights into epithelial morphogenesis in the neonatal mouse uterus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA955822 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24178951.fastq.gz | Fastqsanger.gz | |||
| SRR24178952.fastq.gz | Fastqsanger.gz | |||
| SRR24178953.fastq.gz | Fastqsanger.gz | |||
| SRR24178954.fastq.gz | Fastqsanger.gz | |||
| SRR24178955.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:The uterus is an essential organ for reproduction in mammals, however the cellular and molecular mechanisms that direct its development remain insufficiently understood. To fill this knowledge gap, the epithelium of the neonatal mouse uterus was isolated and subjected to single cell transcriptome (scRNA-seq) analysis. Substantial differences in transcriptional profiles and cell types were evident as the epithelium developed from postnatal days 1 to 15. Both the undifferentiated epithelium and determined luminal epithelium were heterogeneous and contained several different cell clusters. Novel glandular epithelial-specific genes (Gas6 and Cited4) were validated by in situ hybridization during uterine development. Trajectory analyses provided a framework for understanding epithelium maturation and differentiation of the glandular epithelium. A candidate set of transcription factors and gene regulatory networks were identified that regulate epithelium lineage specification and morphogenesis. This atlas provides foundational insights important for future mechanistic studies focused on uterine epithelium morphogenesis during the critical window of postnatal development.
2023-09-14 | GSE229790 | GEO
Project description:Laser capture microdissection coupled with microarray genes expression analysis were utilized in order to elucidate the regulatory networks active in epithelial cells of the neonatal and adult mouse uterus. Genes predominantly expressed in the glandular epithelium (GE) in the neonatal or adult uterus were determined by comparing transcripts in the isolated samples of luminal epithelium (LE) and GE from postnatal day (PD) 10, day of psudopregnancy (DOPP) 2.5 or DOPP 3.5 uteri (n=2/cell type/day).
2013-11-05 | E-GEOD-48239 | biostudies-arrayexpress
Project description:The upper Müllerian duct (MD) is patterned and specified into two morphologically and functionally distinct organs, the oviduct and uterus. It is known that this regionalization process is instructed by inductive signals from the adjacent mesenchyme. However, the interaction landscape between epithelium and mesenchyme during upper MD development remains largely unknown. Here, we performed single-cell transcriptomic profiling of mouse neonatal oviducts and uteri at the initiation of MD epithelial differentiation (postnatal day 3). We identified major cell types including epithelium, mesenchyme, pericytes, mesothelium, endothelium, and immune cells in both organs with established markers. Moreover, we uncovered region-specific epithelial and mesenchymal subpopulations and then deduced region-specific ligand-receptor pairs mediating mesenchymal-epithelial interactions along the craniocaudal axis. Unexpectedly, we discovered a mesenchymal subpopulation marked by neurofilaments with specific localizations at the mesometrial pole of both the neonatal oviduct and uterus. Lastly, we analyzed and revealed organ-specific signature genes of pericytes and mesothelial cells. Taken together, our study enriches our knowledge of upper Müllerian duct development, and provides a manageable list of potential genes, pathways, and region-specific cell subtypes for future functional studies.
2023-12-21 | GSE251724 | GEO
Project description:Laser capture microdissection coupled with microarray genes expression analysis were utilized in order to elucidate the regulatory networks active in epithelial cells of the neonatal and adult mouse uterus.
2013-11-05 | GSE48239 | GEO
Project description:Developmental exposure to diethylstilbestrol (DES) causes reproductive tract malformations, affects fertility and increases the risk of clear cell carcinoma of the vagina and cervix in humans. Previous studies on a well-established mouse DES model demonstrated that it recapitulates many features of the human syndrome, yet the underlying molecular mechanism is far from clear. Using the neonatal DES mouse model, the present study uses global transcript profiling to systematically explore early gene expression changes in individual epithelial and mesenchymal compartments of the neonatal uterus. Over 900 genes show differential expression upon DES treatment in either one or both tissue layers. Interestingly, multiple components of the Peroxisome Proliferator-Activated Receptor gamma (PPAR gamma)-mediated adipogenic/lipid metabolic pathway, including PPARgamma itself, are targets of DES in the neonatal uterus. TEM and Oil Red O staining further demonstrate a dramatic increase in lipid deposition in the uterine epithelial cells upon DES exposure. Neonatal DES exposure also perturbs glucose homeostasis in the uterine epithelium. Some of these neonatal DES-induced metabolic changes appear to last into adulthood, suggesting a permanent effect of DES on energy metabolism in uterine epithelial cells. This study extends the list of biological processes that can be regulated by estrogen or DES, and provides a novel perspective for endocrine disruptor induced reproductive abnormalities.
2012-05-15 | GSE37969 | GEO
Project description:Developmental exposure to diethylstilbestrol (DES) causes reproductive tract malformations, affects fertility and increases the risk of clear cell carcinoma of the vagina and cervix in humans. Previous studies on a well-established mouse DES model demonstrated that it recapitulates many features of the human syndrome, yet the underlying molecular mechanism is far from clear. Using the neonatal DES mouse model, the present study uses global transcript profiling to systematically explore early gene expression changes in individual epithelial and mesenchymal compartments of the neonatal uterus. Over 900 genes show differential expression upon DES treatment in either one or both tissue layers. Interestingly, multiple components of the Peroxisome Proliferator-Activated Receptor gamma (PPAR gamma)-mediated adipogenic/lipid metabolic pathway, including PPARgamma itself, are targets of DES in the neonatal uterus. TEM and Oil Red O staining further demonstrate a dramatic increase in lipid deposition in the uterine epithelial cells upon DES exposure. Neonatal DES exposure also perturbs glucose homeostasis in the uterine epithelium. Some of these neonatal DES-induced metabolic changes appear to last into adulthood, suggesting a permanent effect of DES on energy metabolism in uterine epithelial cells. This study extends the list of biological processes that can be regulated by estrogen or DES, and provides a novel perspective for endocrine disruptor induced reproductive abnormalities. We separated UE from the UM from vehicle (oil)- or DES-treated postnatal day 5 (P5) mice, and prepared biological triplicates of RNA from pooled specimens (nM-bM-^IM-%3). Those samples were analyzed on two MouseWG-6 BeadChips, which detects 45,200 transcripts including more than 26,000 annotated genes in the NCBI RefSeq database. Difference of at least twofold in signal intensity of each given probe set with a P-value less than 0.05 was considered statistically significant.
2012-05-14 | E-GEOD-37969 | biostudies-arrayexpress
Project description:Epithelial differentiation in the female reproductive tract (FRT) is essential for reproductive health, yet the mechanisms that govern epithelial fate specification remain poorly understood. At birth, FRT epithelium exhibits significant developmental plasticity, allowing differentiation into various epithelial subtypes. However, the regulatory pathways driving these early fate decisions, particularly in the uterus, are largely uncharacterized. Here, we employ neonatal mouse endometrial epithelial organoids and assembloid co-culture models to investigate how intrinsic cellular plasticity and mesenchymal signals influence uterine epithelial differentiation. We demonstrate that uterine epithelium undergoes marked age-dependent changes, shifting from a highly plastic state capable of differentiating into both monolayered and multilayered structures to a more restricted fate as development progresses. Interestingly, parallels between the developmental plasticity of neonatal uterine epithelium and pathological conditions such as endometrial cancer emerged, where similar regulatory mechanisms may be reactivated, driving abnormal epithelial differentiation and tumorigenesis. These findings provide new insights into the regulatory networks that guide early development and highlight how disruptions in these processes can contribute to disease, offering a valuable model for studying both normal uterine development and cancer progression.
2025-01-01 | GSE278635 | GEO
Project description:Single-cell transcriptomic profiling of the neonatal oviduct and uterus reveals new insights into upper Müllerian duct regionalization
| PRJNA1055124 | ENA
Project description:BackgroundThe uterus is the location where multiple events occur that are required for the start of new life in mammals. The adult uterus contains endometrial or uterine glands that are essential for female fertility. In the mouse, uterine glands are located in the lateral and antimesometrial regions of the uterine horn. Previous three-dimensional (3D)-imaging of the adult uterus, its glands, and implanting embryos has been performed by multiple groups, using fluorescent microscopy. Adenogenesis, the formation of uterine glands, initiates after birth. Recently, we created a 3D-staging system of mouse uterine gland development at postnatal time points, using light sheet fluorescent microscopy. Here, using a similar approach, we examine the morphological changes in the epithelium of the perinatal mouse uterus.ResultsThe uterine epithelium exhibits dorsoventral (mesometrial-antimesometrial) patterning as early as 3 days after birth (P3), marked by the presence of the dorsally positioned developing uterine rail. Uterine gland buds are present beginning at P4. Novel morphological epithelial structures, including a ventral ridge and uterine segments were identified.ConclusionsThe perinatal mouse uterine luminal epithelium develops dorsal-ventral morphologies at 3 to 4 days postpartum. Between 5 and 6 days postpartum uterine epithelial folds form, defining alternating left-right segments.
| S-EPMC8142688 | biostudies-literature
Project description:Yin Yang 1 (YY1) is a multifunctional zinc-finger-containing transcription factor that plays crucial roles in numerous biological processes by selectively activating or repressing transcription, depending upon promoter contextual differences and specific protein interactions. In mice, Yy1 null mutants die early in gestation while Yy1 hypomorphs die at birth from lung defects. We studied how the epithelial-specific inactivation of Yy1 impacts on lung development. The Yy1 mutation in lung epithelium resulted in neonatal death due to respiratory failure. It impaired tracheal cartilage formation, altered cell differentiation, abrogated lung branching, and caused airway dilation similar to those seen in human congenital cystic lung diseases. The cystic lung phenotype in Yy1 mutants can be explained by the reduced expression of Shh in lung endoderm, a transcriptional target of YY1, and the subsequent derepression of mesenchymal Fgf10 expression. Accordingly, SHH supplementation partially rescued the lung phenotype in vitro. Analysis of human lung tissues revealed decreased YY1 expression in children with pleuropulmonary blastoma (PPB), a rare pediatric lung tumor arising during fetal development and associated with DICER1 mutations. No evidence for a potential genetic interplay between murine Dicer and Yy1 genes during lung morphogenesis was observed. However, the cystic lung phenotype resulting from the epithelial inactivation of Dicer function mimics the Yy1 lung malformations with similar changes in Shh and Fgf10 expression. Together, our data demonstrate the critical requirement for YY1 in lung morphogenesis and identify Yy1 mutant mice as a potential model for studying the genetic basis of PPB.
2015-10-20 | GSE66171 | GEO