Single cell-RNA-seq for airway epithelial cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE111598 | GEO | 2018/03/09
REPOSITORIES: GEO
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Project description:The airway epithelium is in contact with the environment and therefore constantly at risk for injury. Basal cells have been found to repair the surface epithelium, but the contribution of other stem cell populations to airway epithelial repair have not been identified. We demonstrated that airway submucosal gland duct cells, in addition to basal cells, survived severe hypoxic-ischemic injury. We developed a method to isolate duct cells from the airway. In vitro and in vivo models were used to compare the self-renewal and differentiation potential of duct cells and basal cells. We found that only duct cells were capable of regenerating submucosal gland tubules and ducts, as well as the surface epithelium overlying the submucosal glands. This is of importance to the field of lung regeneration as determining the repairing cell populations could lead to the identification of novel therapeutic targets and cell-based therapies for patients with airway diseases.
2012-06-01 | GSE28651 | GEO
Project description:The human airway lining consists of two physiologically distinct compartments: the surface airway epithelium (SAE) and the submucosal glands (SMGs). Despite their critical role, SMGs have remained largely overlooked in airway in vitro modeling of respiratory inflammation and infection. In this study, we leverage long-term cultured organoids derived separately from SAE and SMG to investigate their unique physiological characteristics. Single-cell RNA sequencing (scRNA-seq) analysis confirms that these organoid models accurately replicate the cellular heterogeneity inherent to each tissue type. Specifically, SMG organoids are enriched in MUC5B-producing mucous cells and generate alpha-Smooth Muscle Actin (αSMA)-expressing myoepithelial cells. We identify ANPEP/CD13 as a specific cell surface marker for SMG secretory cells. Exposure to cytokines elicits distinct transcriptomic responses in SMG secretory cells, providing insights into the cellular mechanisms underpinning inflammatory pathogenesis. Infection assays with human alpha-coronavirus 229E (HCoV-229E) reveal a selective vulnerability of CD13-positive secretory cells within SMG organoids, triggering a specific unfolded protein response associated with endoplasmic reticulum (ER) stress. These findings broaden the utility of airway organoids for precision modeling of respiratory (patho-)physiology
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Project description:Submucosal glands (SMGs) in the upper respiratory system of mammals play important roles in fluid secretion, mucociliary transport, and host defense. In people with cystic fibrosis (CF), airway mucus obstruction and SMG duct occlusion are hallmark features. Although intensive investigations have focused on airway surface epithelium in normal and diseased lungs, our knowledge of SMGs is limited in terms of cell biology and physiology. Here, we conducted single cell RNA sequencing (scRNA-seq) of airway SMGs in newborn piglets. First, we dissected individual SMGs and surrounding non-epithelial tissues from newborn non-CF (n = 4) and CF (n = 4) pig trachea. Second, we did scRNA-seq using 10x genomics chromium platform. Third, we processed the raw sequencing data using an improved RefSeq pig genome reference. Last, we integrated all samples together and clustered cells into 14 major cell clusters using Seurat R toolkit (Stuart et al., 2019). These data allowed us to elucidate airway SMGs at single cell resolution. Moreover, we found that cell-types and gene expression were the same in non-CF and CF SMGs, suggesting that loss of epithelial anion secretion rather than an intrinsic cell defect causes CF mucus abnormalities.
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Project description:Repair-supportive mesenchymal cells (RSMCs) have been recently reported in the context of naphthalene (NA)-induced airway injury and regeneration. These cells transiently express smooth muscle actin (Acta2) and are enriched with platelet-derived growth factor receptor alpha (Pdgfra) and fibroblast growth factor 10 (Fgf10) expression. Genetic deletion of Ctnnb1 (gene coding for beta catenin) or Fgf10 in these cells using the Acta2-Cre-ERT2 driver line after injury (defined as NA-Tam condition; Tam refers to tamoxifen) led to impaired repair of the airway epithelium. In this study, we demonstrate that RSMCs are mostly captured using the Acta2-Cre-ERT2 driver when labeling occurs after (NA-Tam condition) rather than before injury (Tam-NA condition), and that their expansion occurs mostly between days 3 and 7 following NA treatment. Previous studies have shown that lineage-traced peribronchial GLI1+ cells are transiently amplified after NA injury. Here, we report that Gli1 expression is enriched in RSMCs. Using lineage tracing with Gli1Cre-ERT2 mice combined with genetic inactivation of Fgf10, we show that GLI1+ cells with Fgf10 deletion fail to amplify around the injured airways, thus resulting in impaired airway epithelial repair. Interestingly, Fgf10 expression is not upregulated in GLI1+ cells following NA treatment, suggesting that epithelial repair is mostly due to the increased number of Fgf10-expressing GLI1+ cells. Co-culture of SCGB1A1+ cells with GLI1+ cells isolated from non-injured or injured lungs showed that GLI1+ cells from these two conditions are similarly capable of supporting bronchiolar organoid (or bronchiolosphere) formation. Single-cell RNA sequencing on sorted lineage-labeled cells showed that the RSMC signature resembles that of alveolar fibroblasts. Altogether, our study provides strong evidence for the involvement of mesenchymal progenitors in airway epithelial regeneration and highlights the critical role played by Fgf10-expressing GLI1+ cells in this context.
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