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. Murine proximal airway duct and basal cells were isolated from 8-12 week old male and female mice and FACS sorted. Each sample contains cells that were sorted from a different pool of 10-15 C57Bl/6 mice. RNA was extracted, labeled, and hybridized to Affymetrix Mouse Genome 430 2.0 Array (GPL1261)
2012-05-31 | E-GEOD-28651 | biostudies-arrayexpress
Project description:One month following airway injury with naphthalene (275mg/kg IP x1 in corn oil), total RNA was isolated from one lobe of the right lung (whole lung) from either Falcor-/- (null) or injured wild-type control mice.
2022-01-31 | GSE126816 | GEO
Project description:To comprehensively study how club cells response to airway epithelial injury, we performed single cell transcriptomic analysis of the normal and NAPH injured lung samples. Our analysis reveals that a previously undescribed pathway promoting mucous metaplasia that involves VEGFa and its receptor KDR. Our single cell RNA sequencing analysis revealed that VEGFR2 (also known as FLK1 or KDR) is expressed in club cell subpopulations. Loss of KDR, its ligand VEGFa, or downstream MEK/ERK causes excessive differentiation of club cells into mucous cells (mainly goblet cells) during development and regeneration following Naphthalene (NAPH) challenge.
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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.
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Project description:Single-cell RNA sequencing of airway submucosal glands in wild-type and cystic fibrosis Pigs
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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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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:We examined how allergic inflammation in early postnatal period influences microglia using a short- and long-term airway allergy model. Male mice (C57BL/6) were immunized by intraperitoneal injection with aluminum hydroxide and ovalbumin (OVA) or phosphate-buffered saline (PBS) (control) at postnatal days (P) 3, 7, and 11, followed by intranasal challenge with OVA or PBS solution twice a week until P30 or P70. Microglia from whole brain were isolated from PBS- and OVA-treated mice by gating on CD11b+CD45int cells with flowcytometry at P30 and P70 respectively. Results suggest the dysregulation of microglial genes related to synaptic pruning and clearance, aging, and corticosteroid pathway and distinction between short- and long- term allergen challenge.
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Project description:Outputs from scRNA seq reads from isolated Mouse E16 and P4 lacrimal glands
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Project description:Matrix metalloproteinase 7 (MMP7) is expressed at low levels in intact, normal airways by non-mucous-producing cells, including ciliated cells. In response to injury and infection, MMP7 expression is quickly and markedly upregulated and functions to regulate wound repair and various mucosal immune processes. We evaluated the global transcriptional response of airway epithelial cells from wild type and Mmp7-null mice cultured at an air-liquid interface. A common injury response was seen in both genotypes with up-regulation of genes associated with proliferation and migration. Analysis of differentially expressed genes between genotypes after injury revealed enrichment of functional categories associated with inflammation, cilia and differentiation. Because these analyses suggested MMP7 regulated ciliogenesis, we evaluated the recovery of the airway epithelium in wild type and Mmp7-null mice in vivo after naphthalene injury. These studies identified a new role for MMP7 in attenuating ciliogenesis during wound repair. A total of 16 air-liquid interface cultures of mouse airway epithelial cells were studied under four conditions: 1. Mmp7-null, no injury (n = 4); 2. Mmp7-null, scratch injury (n = 4); 3. Wildtype, no injury (n =4); 4. Wiltype, scratch injury (n = 4).
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