Esophageal progenitor cell plasticity a 3D organotypic model of epithelial regeneration
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA685350 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13255400.fastq.gz | Fastqsanger.gz | |||
| SRR13255401.fastq.gz | Fastqsanger.gz | |||
| SRR13255346.fastq.gz | Fastqsanger.gz | |||
| SRR13255347.fastq.gz | Fastqsanger.gz | |||
| SRR13255348.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 56 |
Similar Datasets
Project description:Epithelial stem cells are capable of remarkable plasticity, facilitating efficient regenerative responses following damage. Here, we present a versatile model of ectopic niche regeneration that provides evidence of a switch in epithelial stem cell identity as a response to foreign microenvironmental signals. A combination of 3D organotypic cultures, 3D confocal imaging and Next-Generation Sequencing reveal events of epithelial plasticity during the reepithelialization of denuded stroma. In this study we perform a temporal analysis that provides new insights on the mechanisms driving cell fate flexibility in adult epithelial stem cells.
2023-12-14 | GSE163218 | GEO
Project description:Preservation of cell identity is necessary for homeostasis of most adult tissues. This process is challenged every time a tissue undergoes regeneration after stress or injury. In the lethal Duchenne muscular Dystrophy (DMD), skeletal muscle regenerative capacity declines gradually as fibrosis increases. Using genetically engineered-tracing mice, we demonstrate that in dystrophic muscle, specialized cells of muscular, endothelial and hematopoietic origins gain plasticity towards a fibrogenic fate via a TGFβ-mediated pathway. This results in loss of cellular identity and normal function, with deleterious consequences for regeneration. Furthermore, this fibrogenic process involves acquisition of a mesenchymal progenitor multipotent status, illustrating a link between fibrogenesis and gain of progenitor cell functions. As this plasticity was also observed in DMD patients, we propose that mesenchymal transitions impair regeneration and worsen diseases with a fibrotic component. TGFb exposure induced gene expression was measured after 4 days of treatment compared to untreated cells. Three independent experiments were performed both for the treatment and for the control
2015-04-09 | E-GEOD-67687 | biostudies-arrayexpress
Project description:Organotypic human tissue models constitute promising systems to facilitate drug discovery and development. They allow to maintain native cellular phenotypes and functions, which enables long-term pharmacokinetic and toxicity studies, as well as phenotypic screening. To trace relevant phenotypic changes back to specific targets or signaling pathways, comprehensive proteomic profiling is the gold-standard. A multitude of proteomic workflows have been applied on 3D tissue models to quantify their molecular phenotypes; however, their impact on analytical results and biological conclusions has not been evaluated. Here, we compared the performance of twelve mass spectrometry-based global proteomic workflows that differed in the amount of cellular input, lysis protocols and quantification methods for the analysis of primary human liver spheroids. We find that the different protocols differ majorly in the total number and subcellular compartment bias of identified proteins, which is particularly relevant for the reliable quantification of transporters and drug metabolizing enzymes. However, using a model of non-alcoholic fatty liver disease, we show that critical disease pathways are robustly identified using a standardized high throughput-compatible workflow based on thermal lysis, even using only individual spheroids (1,500 cells) as input. The results increase the applicability of proteomic profiling to phenotypic screens in organotypic microtissues and provides a scalable platform for deep phenotyping from limited biological material.
2024-04-29 | PXD047462 | Pride
Project description:Human squamous cell cancers are the most common epithelially derived malignancies. One example is esophageal squamous cell carcinoma (ESCC), which is associated with a high mortality rate that is related to a propensity for invasion and metastasis. We report that periostin, a highly expressed cell adhesion molecule, is a key component of a novel tumor invasive signature obtained from an organotypic culture model of engineered ESCC. This tumor invasive signature classifies with human ESCC microarrays, underscoring its utility in human cancer. Genetic modulation of periostin promotes tumor cell migration and invasion as revealed in gain of and loss of function experiments. Inhibition of EGFR signaling and restoration of wild-type p53 function were each found to attenuate periostin, suggesting interdependence of two common genetic alterations with periostin function. Our studies reveal periostin as an important mediator of ESCC tumor invasion and they indicate that organotypic (3D) culture can offer an important tool to discover novel biologic effectors in cancer. Invading and non-invading genetically engineered human esophageal cells with hTERT and EGFR overexpression and p53 mutations were grown in organotypic culture. These invading and non-invading cells were excised using laser-capture microdissection. RNA was isolated and amplified for Affymetrix U133 microarrays. Subsequent microarray analysis & comparison with 2 independent cohorts of primary ESCC tumors revealed upregulation of periostin as gene with highest upregulation found in novel tumor invasive signature in esophageal cancer.
2010-07-08 | E-GEOD-21293 | biostudies-arrayexpress
Project description:Characterization of 3D-Organotypic Culture of Mouse Adipose-Derived Stem Cells
| PRJNA1041470 | ENA
Project description:Organotypic stromal cells impact endothelial cell transcriptome in 3D microvessel networks
| PRJNA849915 | ENA
Project description:3D Adipose Tissue Culture Links the Organotypic Microenvironment to Improved Adipogenesis
| PRJNA774268 | ENA
Project description:Understanding the molecular underpinnings of adipogenesis is of fundamental importance for the development of novel therapeutics against metabolic disorders. However, translational approaches are hampered as current models do not accurately recapitulate adipogenesis. Here, a scaffold-free versatile 3D adipocyte culture platform with chemically defined conditions is presented in which primary human preadipocytes accurately recapitulate adipogenesis. Following differentiation, multi-omics profiling and functional tests demonstrate that 3D adipocyte cultures feature mature molecular and cellular phenotypes similar to freshly isolated mature adipocytes. Spheroids exhibit physiologically relevant gene expression signatures with 4704 differentially expressed genes compared to conventional 2D cultures (false discovery rate < 0.05), including the concerted expression of factors shaping the adipogenic niche. Furthermore, lipid profiles of >1000 lipid species closely resemble patterns of the corresponding isogenic mature adipocytes in vivo (R^2 = 0.97). Integration of multi-omics signatures with analyses of the activity profiles of 503 transcription factors using global promoter motif inference reveals a complex signaling network, involving YAP, Hedgehog, and TGFβ signaling, that links the organotypic microenvironment in 3D culture to the activation and reinforcement of PPARγ and CEBP activity resulting in improved adipogenesis.
2021-10-27 | GSE186519 | GEO
Project description:The blockage of GABA-A ionotropic channels by means of gabazine is a widespread model of plasticity where the increased synaptic activity triggered by Gabazine leads to the up-regulation of a plethora of activity-dependent genes. Here, we sought to characterize the overall transcriptional response of GABA-A blocking of rat hippocampal organotypic cultures. In each of the three biological replica, half of the organotypic hippocampal cultures derived from two rat littermates were treated with gabazine and compared to the untreated ones in order to determine the set of differentially expressed genes.
2013-05-14 | E-GEOD-46864 | biostudies-arrayexpress
Project description:The blockage of GABA-A ionotropic channels by means of gabazine is a widespread model of plasticity where the increased synaptic activity triggered by Gabazine leads to the up-regulation of a plethora of activity-dependent genes. Here, we sought to characterize the overall transcriptional response of GABA-A blocking of rat hippocampal organotypic cultures.
2013-05-14 | GSE46864 | GEO