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Gene expression data from mouse tracheal mesenchymal cells before and 48hrs after SO2 injury

ABSTRACT: The conducting airway epithelium of the rodent and human lung is underlaid by mesenchymal cells that include vasculature, smooth muscle, fibroblasts and cartilage. The goal of this project is to identify cellular and molecular changes in the mesenchyme after injury to the epithelium by exposure to SO2 and which may participate in repair of the epithelium We used Affymetrix microarray analysis to compare transcripts in tracheal mesenchyme before and after SO2 injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE69057 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA284412

REPOSITORIES: GEO

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Gene expression data from mouse tracheal mesenchymal cells before and 48hrs after SO2 injury

Project description:The conducting airway epithelium of the rodent and human lung is underlaid by mesenchymal cells that include vasculature, smooth muscle, fibroblasts and cartilage. The goal of this project is to identify cellular and molecular changes in the mesenchyme after injury to the epithelium by exposure to SO2 and which may participate in repair of the epithelium We used Affymetrix microarray analysis to compare transcripts in tracheal mesenchyme before and after SO2 injury. Mice tracheal epithelium and mesenchyme were separate for RNA extraction before and 48hrs after SO2 injury. Sample from 4 mice were pooled for each biological experiment. The experiments were repeated three times for triplicate samples.

2016-07-03 | E-GEOD-69057 | biostudies-arrayexpress

Gene expression data from mouse tracheal epithelial cells isolated before and 48hrs after SO2 injury

Project description:The conducting airway epithelium of the rodent and human lung is made up of about equal proportions of ciliated and secretory cells. In addition, in regions where the epithelium is pseudostratfied, ~30% of the epithelium consists of undifferentiated basal cells (BCs). Evidence suggests that these BCs are multipotent stem cells that can self renew over the long term and give rise to both ciliated and secretory lineages. The goal of this project is to identify cellular and molecular mechanisms by which the basal cells normally maintain the epithelium and repair it after injury. We used Affymetrix microarray analysis to compare transcripts in tracheal epithelium before and after SO2 injury. Mice tracheal epithelium and mesenchyme were separate for RNA extraction before and 48hrs after SO2 injury. Cells from tracheas of 4 male C57Bl/6 mice were pooled for each biological experiment. The experiments were repeated three times for triplicate samples.

2016-07-03 | E-GEOD-69056 | biostudies-arrayexpress

Gene expression data from mouse tracheal epithelial cells isolated before and 48hrs after SO2 injury

2016-01-01 | GSE69056 | GEO

Gene expression data from mouse tracheal cells before and 48hrs after SO2 injury

Project description:Gene expression data from mouse tracheal cells before and 48hrs after SO2 injury

| PRJNA284410 | ENA

Cartilage rings contribute to the proper embryonic tracheal epithelial differentiation, metabolism and expression of inflammatory genes

Project description:The signaling crosstalk between the tracheal mesenchyme and epithelium has not been researched extensively leaving a substantial gap of knowledge in the mechanisms dictating embryonic development of the proximal airways by the adjacent mesenchyme. Recently, we have reported that embryos lacking mesenchymal expression of Sox9 did not develop tracheal cartilage rings and showed aberrant differentiation of the tracheal epithelium. Herein, we propose that tracheal cartilage provides local inductive signals responsible for the proper differentiation, metabolism, and inflammatory status regulation of the tracheal epithelium. The tracheal epithelium of mesenchyme-specific Sox9D/D mutants showed altered mRNA expression of various epithelial markers such as Pb1fa1, Sftpb, Scgb1a1, and Tff-1. In vitro tracheal epithelial cell cultures confirmed that tracheal chondrocytes secrete factors that inhibit club cell differentiation. Whole gene expression profiling and ingenuity pathway analysis showed that the TNF-a, IFN-g and TGF-b signaling pathways were significantly altered in the Sox9 mutant trachea. Tnf-a and Ifn-g interfered with the differentiation of tracheal epithelial progenitor cells into mature epithelial cell types in vitro. Meanwhile, mesenchymal knockout of Tgf-b1 in vivo resulted in altered differentiation of the tracheal epithelium. Finally, mitochondrial enzymes involved in fat and glycogen metabolism Cox8b and Cox7a1 were strongly up-regulated in the Sox9 mutant trachea, with consequently increased number and size of glycogen storage vacuoles. Our results support an a role for tracheal cartilage in the modulation of the differentiation and metabolism, and the expression of inflammatory related genes in the tracheal epithelium by feeding into the TNF-a, IFN-g and TGF-b signaling pathways.

2017-04-14 | GSE97788 | GEO

Airway-Associated Macrophages in Homeostasis and Repair

Project description:We isolated CD45+ cells after injury (Uninjured, Day1, Day4 and Day7) and CD45+F4/80+ cells from tracheal mesenchyme and dissociated lung, as well as CD45+ cells from peeled tracheal epithelium.

2020-12-30 | GSE152501 | GEO

NDR kinase Tricornered genetically interacts with Ccm3 and metabolic enzymes in Drosophila melanogaster tracheal development

Project description:The GckIII pathway is a Hippo-like kinase module defined by sequential activation of Ste20 kinases Thousand and One (Tao) and Germinal Center Kinase III (GckIII), followed by nuclear dbf2-related (NDR) kinase Tricornered (Trc). We previously uncovered a role for the GckIII pathway in regulating tube morphology in the Drosophila melanogaster tracheal (respiratory) system. The trachea form a network of branched epithelial tubes essential for oxygen transport, and are structurally analogous to branched tubular organs in vertebrates, such as the vascular system. In the absence of GckIII pathway function, aberrant dilations form in tracheal tubes characterised by mislocalized junctional and apical proteins, suggesting that the GckIII pathway is important in maintaining tube integrity in development. Here, we observed a genetic interaction between trc and Cerebral cavernous malformations 3 (Ccm3), the Drosophila ortholog of a human vascular disease gene, supporting our hypothesis that the GckIII pathway functions downstream of Ccm3 in trachea, and potentially in the vertebrate cerebral vasculature. However, how GckIII pathway signalling is regulated and the mechanisms that underpin its function in tracheal development are unknown. We undertook biochemical and genetic approaches to identify proteins that interact with Trc, the most downstream GckIII pathway kinase. We found that known GckIII and NDR scaffold proteins are likely to control GckIII pathway signalling in tracheal development, consistent with their conserved roles in Hippo-like modules. Furthermore, we show genetic interactions between trc and multiple enzymes in glycolysis and oxidative phosphorylation, suggesting a potential function of the GckIII pathway in integrating cellular energy requirements with maintenance of tube integrity.

2023-03-13 | PXD038912 | Pride

Gene expression data from mouse tracheal cells before and 48hrs after SO2 injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-01-01 | GSE69058 | GEO

Mycoplasmopsis synoviae strain:tracheal swab | isolate:tracheal swab

Project description:Mycoplasmopsis synoviae strain:tracheal swab | isolate:tracheal swab Genome sequencing

| PRJNA1009207 | ENA

mTOR Inhibition Enables Long-Term Expansion of Human Neonatal Tracheal Aspirate-Derived Airway Basal Stem Cells

Project description:Bronchopulmonary dysplasia remains one of the most common complication of prematurity, despite significant improvements in perinatal care. Functional modeling of human lung development and disease, like BPD, is limited by our ability to access the lung and to maintain relevant stem cell populations in culture. Single cell RNA-sequencing confirmed the presence of epithelial cells in tracheal aspirates obtained from intubated neonates. Using combined SMAD signaling inhibition and mTOR inhibition neonatal tracheal-aspirate derived (nTAD) basal stem cells can be expanded long-term and retain the ability to differentiate into pseudo-stratified airway epithelium. Conclusions: Our data demonstrate that neonatal tracheal aspirate-derived epithelial cells can provide a novel ex vivo human cellular model to study neonatal lung development and disease.

2020-09-21 | GSE137950 | GEO

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