Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA277526 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1852851_1.fastq.gz | Fastqsanger.gz | |||
| SRR1852851_2.fastq.gz | Fastqsanger.gz | |||
| SRR1852853_1.fastq.gz | Fastqsanger.gz | |||
| SRR1852853_2.fastq.gz | Fastqsanger.gz | |||
| SRR1852854_1.fastq.gz | Fastqsanger.gz |
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Project description:Cross-species transcriptome profiling identifies new alveolar epithelial type I cell-specific genes
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Project description:Diseases involving the distal lung alveolar epithelium include chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and lung adenocarcinoma. Accurate labeling of specific cell types is critical for determining the contribution of each to pathogenesis of these diseases. The distal lung alveolar epithelium is comprised of two cell types, alveolar epithelial type 1 (AT1) and type 2 (AT2) cells. While cell type-specific markers, most prominently surfactant protein C (SFTPC), have allowed detailed lineage tracing studies of AT2 cell differentiation and their roles in disease, studies of AT1 cells have been hampered by lack of genes with expression unique to AT1 cells. In this study, we performed genome-wide expression profiling of multiple rat organs alongside purified rat AT2, AT1 and in vitro differentiated AT1-like cells, resulting in identification of 54 candidate AT1 cell markers. Cross-referencing with genes upregulated in human in vitro differentiated AT1-like cells narrowed the potential list to 18 candidate genes. Testing the top four candidate genes at RNA and protein levels revealed GRAM domain 2 (GRAMD2), a protein of unknown function, as highly specific to AT1 cells. RNAseq confirmed that GRAMD2 is transcriptionally silent in human AT2 cells. Immunofluorescence verified that GRAMD2 expression is restricted to the plasma membrane of AT1 cells and is not expressed in bronchial epithelial cells, while RT-PCR confirmed that it is not expressed in endothelial cells. Utilizing GRAMD2 as a new AT1 cell-specific gene will enhance AT1 cell isolation, investigation of alveolar epithelial cell differentiation potential, and contribution of AT1 cells to distal lung diseases.
2016-11-03 | GSE59120 | GEO
Project description:Diseases involving the distal lung alveolar epithelium include chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and lung adenocarcinoma. Accurate labeling of specific cell types is critical for determining the contribution of each to pathogenesis of these diseases. The distal lung alveolar epithelium is comprised of two cell types, alveolar epithelial type 1 (AT1) and type 2 (AT2) cells. While cell type-specific markers, most prominently surfactant protein C (SFTPC), have allowed detailed studies of AT2 cell differentiation and their roles in disease, studies of AT1 cells have been hampered by lack of genes with expression unique to AT1 cells. To address this, we performed genome-wide expression profiling of multiple rat organs alongside purified rat AT2, AT1 and in vitro differentiated AT1-like cells, resulting in identification of 54 candidate AT1 cell markers. Cross-referencing with genes upregulated in human in vitro differentiated AT1-like cells narrowed the potential list to 18 candidate genes. Testing the top four candidate genes at RNA and protein levels revealed GRAM domain 2 (GRAMD2), a protein of unknown function, as unique to AT1 cells, while SCNN1G within lung is restricted to AT1 cells. RNAseq confirmed that GRAMD2 is transcriptionally silent in human AT2 cells. Immunofluorescence of mouse alveoli verified that GRAMD2 expression is restricted to the plasma membrane of AT1 cells. These new AT1 cell-specific genes, with GRAMD2 as a leading candidate, will enhance AT1 cell isolation, investigation of alveolar epithelial cell differentiation potential, and contribution of AT1 cells to distal lung diseases.
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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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