Similar Datasets
Project description:Single cell transcriptomic profile of human airway orgnaoids.
| PRJNA919922 | ENA
Project description:Extracellular vesicle (EV)-mediated intercellular communication significantly influences pulmonary cell health and disease outcomes, yet in vitro methods to investigate these pathophysiological mechanisms are limited. We hypothesize that organotypic models of the airway can be leveraged to investigate EV-mediated intercellular signaling, focusing on EV proteomic content as a case study. in this study, two in vitro airway culture models were evaluated using mass spectrometry-based proteomics: a tri-culture model consisting of alveolar epithelial, fibroblast, and lung microvascular endothelial cells and a co-culture model consisting of alveolar epithelial and fibroblast cells. EVs isolated from the tri-culture model showed enrichment for EV proteins regulating RNA-to-protein translation. EVs isolated from the co-culture model were enriched with EV biogenesis and extracellular matrix signaling proteins. These model-specific differences suggest that different pulmonary cell types uniquely affect EV composition and the biological pathways influenced by the EV proteome in recipient cells. These findings inform future study designs surrounding EV-related pulmonary disease pathogenesis and therapeutics.
2024-01-26 | PXD040470 | Pride
Project description:Bulk RNA sequencing was performed on intestinal and airway organoids. Also airway organoid derived air-liquid interface cultures were sequenced
2021-08-17 | GSE181514 | GEO
Project description:Micro-patterned culture of iPSC-derived airway epithelial cells [airway]
| PRJNA992510 | ENA
Project description:Airway organoids derived from adult murine epithelial cells represent a complex 3D in vitro system mimicking the airway epithelial tissue’s native cell composition and physiological properties. In combination with a precise damage induction via femtosecond laser-based nanosurgery, this model allows for the examination of intra- and intercellular dynamics in the course of repair processes with a high spatio-temporal resolution, which can hardly be reached using in vivo approaches. For characterization of the organoids’ response to single or multiple-cell ablation, we first analyzed overall organoid survival and found that airway organoids were capable of efficiently repairing damage induced by femtosecond laser-based ablation of a single to ten cells within 24 h. An EdU staining assay further revealed a steady proliferative potential of airway organoid cells. Especially in the case of ablation of five cells, proliferation was enhanced within the first four hours upon damage induction, whereas ablation of ten cells was followed by a slight decrease in proliferation within this time frame. Analyzing individual trajectories of single cells within airway organoids, we found an increased migratory behavior in cells within close proximity to the ablation site following the ablation of ten, but not five cells. Bulk RNA sequencing and subsequent enrichment analysis revealed the differential expression of sets of genes involved in the regulation of epithelial repair, distinct signaling pathway activities such as Notch signaling, as well as cell migration after laser-based ablation. Together, our findings demonstrate that organoid repair upon ablation of ten cells involves the same key processes by which native airway epithelial wound healing is regulated. This marks the herein presented in vitro damage model suitable to study repair processes following acute airway injury, thereby posing a novel approach to gain insights into the mechanisms driving epithelial repair on a single-cell level.
2023-08-29 | GSE241237 | GEO
Project description:The purpose of the study is to compare the transcriptomic profile of the airway epithelium generated from bronchial airway epithelial cells isolated from healthy donors (NCF) and patients with cystic fibrosis (CF). Cells were grown at the air-liquid interface for at least 2-months. CF is caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Only patients homozygous for the F508del mutation of the CFTR gene were considered. The reconstituted airway epithelium was mechanically wounded and allowed to repair with time. We considered four steps: 1) intact, non-wounded (NW) epithelium; 2) 24h hours post-wounding (pW); 3) time at which the wound is closed (WC); 4) two days post-wound closure (pWC). We also mimicked infection by exposing the cells to Pseudominas aeruginosa flagelin for NW and WC conditions.
2019-10-08 | GSE127696 | GEO
Project description:Three patient-derived organoids from liver metastasis of CRC samples were profiled by scRNA-seq.
2024-02-29 | E-MTAB-13123 | biostudies-arrayexpress
Project description:Many lung diseases remain understudied due to a lack of experimental models. Lung organoids, which consist of self-organizing epithelial cells, provide versatile in vitro models for normal and abnormal biology, drug screening, gene editing, and personalized therapeutics. However, human organoids are generally derived from lung tissue, which is not commonly obtained and represents only a small fraction of lung pathologies. Induced pluripotent stem cells have provided an important alternative but require complex manipulation. Recently, one study reported airway organoids from bronchoalveolar lavage (BAL) fluid, though sample sizes and characterization were limited. Here, we demonstrate robust establishment of airway organoids from a variety of human BAL samples and show that these organoids consist predominantly of basal cells plus differentiated airway cell types including secretory, ciliated, KRT13+ “hillock,” and ionocyte cells. Furthermore, we report the development of BAL-derived alveolar organoids comprised of alveolar type 2 (AT2) cells. These techniques significantly expand the scope of lung diseases that can be studied using safely accessible primary human cells.
2024-05-01 | GSE254166 | GEO
Project description:BACKGROUND: We have previously reported gene expression changes in the bronchial airway epithelium of active chronic smokers. In this study, we investigate the effects of Acute Smoke Exposure (ASE) from cigarettes on airway epithelial gene expression. METHODS: Bronchial airway epithelial cell brushings were collected via fiberoptic bronchoscopy from 63 individuals without recent exposure to cigarette smoke (> 2 days), at baseline and at 24 hours after smoking three cigarettes. RNA from these samples was profiled on Affymetrix Human Gene 1.0 ST microarrays. Differential gene expression was assessed using linear modeling and compared to previous smoking-related gene-expression signatures using Gene Set Enrichment Analysis (GSEA). RESULTS: We identified 91 genes differentially expressed 24-hours after exposure to three cigarettes (FDR < 0.25). ASE induces genes involved in xenobiotic metabolism, oxidative stress, and inflammation; and represses genes involved in cilium morphogenesis, and cell cycle. Genes induced by in vivo ASE are concordantly altered by ASE in vitro. While many genes altered by ASE are altered similarly in the airway of chronic smokers, metallothionein genes were induced by ASE and suppressed among chronic smokers. Metallothioneins were also suppressed in the bronchial airway of current and former chronic smokers with lung cancer relative to those with benign disease. CONCLUSIONS: Acute exposure to as little as three cigarettes alters gene-expression in bronchial airway epithelium in a manner that largely resembles the changes seen in chronic active smokers. The difference in the short-term and long-term effects of smoking on metallothionein expression and its relationship to lung cancer requires further study given these enzymes’ role in responding to oxidative stress.
2018-06-26 | GSE97010 | GEO
Project description:We established a micro-patterned respiratory epithelial cell culture system in vitro. In this culture system, the iPSC-derived lung progenitor cells were differentiated into airway epithelial cells in a position-specific manner.
2024-02-29 | GSE236840 | GEO