Ontology highlight
ABSTRACT:
PROVIDER: PRJNA897704 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22164060_1.fastq.gz | Fastqsanger.gz | |||
| SRR22164060_2.fastq.gz | Fastqsanger.gz | |||
| SRR22164061_1.fastq.gz | Fastqsanger.gz | |||
| SRR22164061_2.fastq.gz | Fastqsanger.gz | |||
| SRR22164062_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:Spatial regulation of the glycocalyx component Podocalyxin is a switch for pro-metastatic function
| PRJEB53371 | ENA
Project description:Embryo implantation is a key step in establishing pregnancy and a major limiting factor in IVF. Implantation requires the endometrium, the inner lining of the uterus, to transform from a non-receptive to a receptive state, to allow embryos to attach to the surface and enter into the tissue. However, the fundamental mechanisms governing receptivity are not well understood. Here we show that transmembrane protein podocalyxin is a major and clinically significant factor regulating human endometrial receptivity. Podocalyxin is expressed in all endometrial epithelial cells in the non-receptive state but is selectively down-regulated in the luminal epithelium at receptivity. We present evidence that podocalyxin critically governs the barrier function of the endometrial epithelium, likely as an intrinsic protective mechanism, rendering it non-receptive to an embryo. In addition, podocalyxin suppresses genes promoting receptivity (eg LIF, CSF1) but stimulates those inhibiting implantation (eg WNT7A, LEFTY2). Down-regulation of podocalyxin in the luminal epithelium, likely mediated by progesterone, selectively converts the endometrial surface to a more adhesive state that facilitates embryo attachment and penetration. Furthermore, inadequate down-regulation of podocalyxin in the endometrial luminal epithelium is associated with poorer implantation rates in IVF. We thus propose that podocalyxin promotes the barrier function of human endometrial epithelial cells and critically regulates receptivity for embryo implantation.
2021-04-01 | GSE148274 | GEO
Project description:The glycocalyx consists of glycoproteins, glycolipids and extracellular polysaccharides at the cell surface which mediate viscoelastic and electrostatic barrier function. In molecular interactions the glycocalyx is thought to segregate locally to facilitate receptor-ligand binding, yet high-resolution maps of glycocalyx domains in cell-cell and cell-matrix interactions are lacking. We here applied TMTH-sulfoximine (THS)-based biorthogonal chemistry in live-cell culture and demonstrate much-enhanced glycocalyx detection, compared to established dibenzocyclooctyne-based labeling. Using superresolution microscopy, we identified micron-scale moderately diminished glycocalyx in cell-cell contacts and subtotal depletion in protrusions at the leading and trailing edges and membrane blebs when cells invaded 3D fibrillar matrix. At contacts to collagen fibrils, focal integrin clusters segregated in outward-protrusive nanodomains from glycocalyx (distance: 350 nm), forming adhesion sites of low glycocalyx content. Thus, THS-based next-generation bioorthogonal labelling of live cells identifies micro- and nanodomains with altered glycocalyx density, implicating local glycocalyx downregulation in functional cell-cell and cell-matrix interactions.
2025-03-18 | GSE287160 | GEO
Project description:Abstract:
Accumulating experimental and clinical evidence suggest that the immune response to cancer is not exclusively anti-tumor. Indeed, the pro-tumor roles of the immune system - as suppliers of growth and pro-angiogenic factors or defenses against cytotoxic immune attacks, for example - have been long appreciated, but relatively few theoretical works have considered their effects. Inspired by the recently proposed "immune-mediated" theory of metastasis, we develop a mathematical model for tumor-immune interactions at two anatomically distant sites, which includes both anti- and pro-tumor immune effects, and the experimentally observed tumor-induced phenotypic plasticity of immune cells (tumor "education" of the immune cells). Upon confrontation of our model to experimental data, we use it to evaluate the implications of the immune-mediated theory of metastasis. We find that tumor education of immune cells may explain the relatively poor performance of immunotherapies, and that many metastatic phenomena, including metastatic blow-up, dormancy, and metastasis to sites of injury, can be explained by the immune-mediated theory of metastasis. Our results suggest that further work is warranted to fully elucidate the pro-tumor effects of the immune system in metastatic cancer.
2024-09-02 | BIOMD0000000926 | BioModels
Project description:The intestine is under constant exposure to chemicals, antigens and microorganisms from the external environment. Apical aspects of absorptive epithelial cells form a brush border membrane (BBM), shaped by packed microvilli coated with a dense glycocalyx. We present evidence showing that the glycocalyx forms an epithelial barrier that prevents exogenous molecules and live bacteria from gaining access to BBM. We used a multi-omics approach to investigate function and regulation of membrane mucins exposed on the BBM during postnatal development of the mouse small intestine. Muc17 was identified as a major membrane mucin in the glycocalyx that was specifically upregulated by IL-22 as part of an epithelial defense repertoire during weaning. High levels of IL-22 at time of weaning reprogrammed neonatal postmitotic progenitor enterocytes to differentiate into Muc17-expressing enterocytes, as found in adult intestine during homeostasis. Our findings propose a role for Muc17 in epithelial barrier function in small intestine.
2021-02-16 | GSE164552 | GEO
Project description:After birth, the intestine undergoes major changes to shift from an immature proliferative state to a functional intestinal barrier. By combining inducible lineage tracing and transcriptomics in mouse models, we identify a pro-differentiation PDGFRαHigh intestinal stromal lineage originating from postnatal LTβR+ perivascular stromal progenitors. Genetic blockage of this lineage increased the intestinal stem cells pool while decreasing epithelial and immune maturation at weaning age, leading to reduced postnatal growth and dysregulated repair responses. Ablating PDGFRα in the LTβR stromal lineage demonstrates that PDGFRα has a major impact on the lineage fate and function, inducing a transcriptomic switch from pro-stemness genes such as Rspo3 and Grem1 to pro-differentiation factors including BMPs, retinoic acid and laminins, and on spatial organization within the crypt-villus and repair responses. Our results show that PDGFRα-induced transcriptomic switch in intestinal stromal cells is required in the first weeks after birth to coordinate postnatal intestinal maturation and function.
2022-05-05 | GSE200364 | GEO
Project description:After birth, the intestine undergoes major changes to shift from an immature proliferative state to a functional intestinal barrier. By combining inducible lineage tracing and transcriptomics in mouse models, we identify a pro-differentiation PDGFRαHigh intestinal stromal lineage originating from postnatal LTβR+ perivascular stromal progenitors. Genetic blockage of this lineage increased the intestinal stem cells pool while decreasing epithelial and immune maturation at weaning age, leading to reduced postnatal growth and dysregulated repair responses. Ablating PDGFRα in the LTβR stromal lineage demonstrates that PDGFRα has a major impact on the lineage fate and function, inducing a transcriptomic switch from pro-stemness genes such as Rspo3 and Grem1 to pro-differentiation factors including BMPs, retinoic acid and laminins, and on spatial organization within the crypt-villus and repair responses. Our results show that PDGFRα-induced transcriptomic switch in intestinal stromal cells is required in the first weeks after birth to coordinate postnatal intestinal maturation and function.
2022-05-05 | GSE200363 | GEO
Project description:After birth, the intestine undergoes major changes to shift from an immature proliferative state to a functional intestinal barrier. By combining inducible lineage tracing and transcriptomics in mouse models, we identify a pro-differentiation PDGFRαHigh intestinal stromal lineage originating from postnatal LTβR+ perivascular stromal progenitors. Genetic blockage of this lineage increased the intestinal stem cells pool while decreasing epithelial and immune maturation at weaning age, leading to reduced postnatal growth and dysregulated repair responses. Ablating PDGFRα in the LTβR stromal lineage demonstrates that PDGFRα has a major impact on the lineage fate and function, inducing a transcriptomic switch from pro-stemness genes such as Rspo3 and Grem1 to pro-differentiation factors including BMPs, retinoic acid and laminins, and on spatial organization within the crypt-villus and repair responses. Our results show that PDGFRα-induced transcriptomic switch in intestinal stromal cells is required in the first weeks after birth to coordinate postnatal intestinal maturation and function.
2022-05-05 | GSE200362 | GEO
Project description:Loss of the Endothelial Glycocalyx Component EMCN Leads to Glomerular Impairment
| PRJNA1131386 | ENA
Project description:The apical aspects of absorptive epithelial cells form a highly organized brush border membrane (BBM), shaped by densely packed microvilli that are coated with a glycocalyx. Here, we present evidence showing that the glycocalyx forms an epithelial barrier that prevents exogenous molecules from gaining access to the BBM. We used a multiomics approach to investigate function and regulation of membrane mucins exposed on the enterocytic BBM during postnatal development of the small intestine. Muc17 was identified as a major membrane mucinin the glycocalyx that was specifically upregulated by IL-22 as part of an epithelial defense repertoire during suckling-weaning transition. High levels of IL-22 at the time of weaning primed progenitor enterocyte to express Muc17 as they migrate out of intestinal crypts to replace neonatal enterocytes. Our findings propose a role for membrane mucin Muc17 in epithelial barrier function in the small intestine.
2021-02-16 | PXD018592 | Pride