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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

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

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

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

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

2020-04-15 | GSE137353 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-03 | E-GEOD-69058 | biostudies-arrayexpress

Transcriptional signature of murine tracheal brush cells identified by RNA-Seq

Project description:Purpose: Tracheal epithelial brush cells are rare chemosensory cells defined by their expression of elements of the bitter taste transduction system, and known to activate the cholinergic nervous system in the murine lung. Similar chemosensory cells in the intestine can generate lipid mediators and pro-inflammatory cytokines but whether brush cell can contribute to airway inflammation is unknown. Furthermore, despite the advances in understanding chemosensory cell effector functions, the receptors that mediate chemosensory cell activation and expansion beyond taste receptors in any compartment remain largely unknown. Methods: In this study, we isolated tracheal brush cells by FACS from naïve ChATBAC-eGFP mice with knockin of eGFP within a BAC spanning the acetylcholine transferase locus, marking brush cells in the epithelium and performed transcriptome profiling using low input RNA sequencing. We compared tracheal brush cells to EpCAM+ epithelial cells and CD45+ hematopoetic cells in naive mice. Results: When compared to EpCAM+ EpCs and to CD45+ cells in the airway, principal component analysis demonstrated that brush cells grouped quite distinctly. This brush cell distinction relative to EpCAM+ cells, was further reflected in the striking number of highly differentially expressed genes. This included 1305 genes expressed at 4-fold or higher levels in EpCAM+eGFP+ cells (brush cells), of which 418 genes were expressed at 32-fold or higher levels in brush cells. Conclusions: Our study represents the first detailed analysis of the transcriptome of tracheal brush cells and identifies a unique set of genes that are primarily expressed in brush cells including the bitter taste transduction system, synthenic machinery for several pro-inflammatory lipid mediators and HoxA2 transciptional factors.

2018-07-03 | GSE116525 | GEO

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