Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA380617 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5379120_1.fastq.gz | Fastqsanger.gz | |||
| SRR5379120_2.fastq.gz | Fastqsanger.gz | |||
| SRR5379121_1.fastq.gz | Fastqsanger.gz | |||
| SRR5379121_2.fastq.gz | Fastqsanger.gz | |||
| SRR5379122_1.fastq.gz | Fastqsanger.gz |
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Project description:Regeneration of the lung alveolus by an evolutionarily conserved epithelial progenitor [mouse RNA-seq]
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Project description:The lung alveolus is the primary site of gas exchange in mammals. Within the alveolus, the alveolar type 2 (AT2) epithelial cell population generates surfactant to maintain alveolar structure and harbors a regenerative capacity to repair the alveolus after injury. We show that a Wnt-responsive alveolar epithelial progenitor (AEP) lineage within the AT2 cell population is critical for regenerating the alveolar niche. AEPs are a stable lineage during alveolar homeostasis but expand rapidly to regenerate a majority of the alveolar epithelium after acute lung injury. AEPs exhibit a distinct transcriptome, epigenome, and functional phenotype with specific responsiveness to Wnt and FGF signaling that modulates differentiation and self-renewal, respectively. Importantly, human AEPs (hAEPs) can be isolated and characterized through a conserved surface marker and are required for human alveolar self-renewal and differentiation using alveolar organoid assays. Together, our findings show that AEPs are an evolutionarily conserved alveolar progenitor lineage essential for regenerating the alveolar niche in the mammalian lung.
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Project description:The lung alveolus is the primary site of gas exchange in mammals. Within the alveolus, the alveolar type 2 (AT2) epithelial cell population generates surfactant to maintain alveolar structure and harbors a regenerative capacity to repair the alveolus after injury. We show that a Wnt-responsive alveolar epithelial progenitor (AEP) lineage within the AT2 cell population is critical for regenerating the alveolar niche. AEPs are a stable lineage during alveolar homeostasis but expand rapidly to regenerate a majority of the alveolar epithelium after acute lung injury. AEPs exhibit a distinct transcriptome, epigenome, and functional phenotype with specific responsiveness to Wnt and FGF signaling that modulates differentiation and self-renewal, respectively. Importantly, human AEPs (hAEPs) can be isolated and characterized through a conserved surface marker and are required for human alveolar self-renewal and differentiation using alveolar organoid assays. Together, our findings show that AEPs are an evolutionarily conserved alveolar progenitor lineage essential for regenerating the alveolar niche in the mammalian lung.
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Project description:The lung alveolus is the primary site of gas exchange in mammals. Within the alveolus, the alveolar type 2 (AT2) epithelial cell population generates surfactant to maintain alveolar structure and harbors a regenerative capacity to repair the alveolus after injury. We show that a Wnt-responsive alveolar epithelial progenitor (AEP) lineage within the AT2 cell population is critical for regenerating the alveolar niche. AEPs are a stable lineage during alveolar homeostasis but expand rapidly to regenerate a majority of the alveolar epithelium after acute lung injury. AEPs exhibit a distinct transcriptome, epigenome, and functional phenotype with specific responsiveness to Wnt and FGF signaling that modulates differentiation and self-renewal, respectively. Importantly, human AEPs (hAEPs) can be isolated and characterized through a conserved surface marker and are required for human alveolar self-renewal and differentiation using alveolar organoid assays. Together, our findings show that AEPs are an evolutionarily conserved alveolar progenitor lineage essential for regenerating the alveolar niche in the mammalian lung.
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Project description:Epithelial cells that are committed to a differentiated state in homeostasis can change their identity in response to injury. In the lung, alveolar type 2 (AT2) cells are the resident secretory epithelial cells of the alveolus, and after injury can proliferate and differentiate into type 1 cells. This inducible plasticity is central to alveolar regeneration, fibrosis, and malignancy, but the regulatory pathways that govern the balance between fate maintenance and differentiation are incompletely understood. Epithelial cells that are committed to a differentiated state in homeostasis can change their identity in response to injury. In the lung, alveolar type 2 (AT2) cells are the resident secretory epithelial cells of the alveolus, and after injury can proliferate and differentiate into type 1 cells. This inducible plasticity is central to alveolar regeneration, fibrosis, and malignancy, but the regulatory pathways that govern the balance between fate maintenance and differentiation are incompletely understood. IRE1α is an ER transmembrane protein conserved throughout eukaryotes that senses misfolded protein in the ER lumen and initiates cellular efforts to regain protein folding homeostasis through its cytosolic kinase and RNase domains. We previously showed that IRE1α pharmacologic or genetic loss of function decreased the accumulation of damage-associated transient progenitors (DATPs), and also promoted their differentiation into new alveolar epithelial cells. To further detail the functions of IRE1α after AT2 injury, we performed single-cell transcriptome profiling of the AT2-to-AT1 transition after bleomycin injury, with pharmacologic or epithelial-specific genetic loss of IRE1α function.
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Project description:We have employed a single cell sequencing approach using 10x Genomics scRNAseq to study Cdh16-expression alveolar epithelial progenitor during mouse lung development. Alveolar morphogenesis and regeneration rely on progenitors to replenish alveolar epithelia. Cdh16 positive cells constitute an epithelial progenitor pool capable of differentiating into both AT2 and AT1 cells.In this study, we present the first scRNA-seq analysis on of Cdh16 lineage traced cells during mouse lung alveologenesis, revealing their plasticity with a dynamic differentiation trajetory along with the embryonic stages as well as the postnatal days. Overall, our study elucidates the crucial role of the Cdh16 lineage as alveolar epithelial progenitors in lung development and regeneration.
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