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Interleukin-17 governs hypoxic adaptation of injured epithelium [CITE-seq & single-cell RNA-seq]

ABSTRACT: Interleukin-17 governs hypoxic adaptation of injured epithelium [CITE-seq & single-cell RNA-seq]

PROVIDER: PRJNA702457 | ENA |

REPOSITORIES: ENA

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Interleukin-17 governs hypoxic adaptation of injured epithelium

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium

| PRJNA702447 | ENA

Interleukin-17 governs hypoxic adaptation of injured epithelium [spatial transcriptomics]

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium [spatial transcriptomics]

| PRJNA702458 | ENA

Interleukin-17 governs hypoxic adaptation of injured epithelium [bulk RNA-seq]

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium [bulk RNA-seq]

| PRJNA702456 | ENA

Interleukin-17 governs hypoxic adaptation of injured epithelium [CITE-seq & single-cell RNA-seq]

Project description:To define the composition of “first responder” lymphocytes that may engage in crosstalk with injured epithelium we profiled the lymphoytes from unwounded health skin and skin from different time points after wounding with CITE-seq and single-cell RNA-sequencing.

2021-02-18 | GSE166949 | GEO

Interleukin-17 governs hypoxic adaptation of injured epithelium.

Project description:Mammalian cells autonomously activate hypoxia-inducible transcription factors (HIFs) to ensure survival in low-oxygen environments. We report here that injury-induced hypoxia is insufficient to trigger HIF1α in damaged epithelium. Instead, multimodal single-cell and spatial transcriptomics analyses and functional studies reveal that retinoic acid-related orphan receptor γt+ (RORγt+) γδ T cell-derived interleukin-17A (IL-17A) is necessary and sufficient to activate HIF1α. Protein kinase B (AKT) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling proximal of IL-17 receptor C (IL-17RC) activates mammalian target of rapamycin (mTOR) and consequently HIF1α. The IL-17A-HIF1α axis drives glycolysis in wound front epithelia. Epithelial-specific loss of IL-17RC, HIF1α, or blockade of glycolysis derails repair. Our findings underscore the coupling of inflammatory, metabolic, and migratory programs to expedite epithelial healing and illuminate the immune cell-derived inputs in cellular adaptation to hypoxic stress during repair.

| S-EPMC9753231 | biostudies-literature

Interleukin-17 governs hypoxic adaptation of injured epithelium

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-18 | GSE166950 | GEO

Interleukin-17 governs hypoxic adaptation of injured epithelium [spatial transcriptomics]

Project description:To define the gene signature and spatial architecture of the skin after injury, we performed spatial transcriptomics from mouse unwounded and wounded skin.

2021-02-18 | GSE166948 | GEO

Interleukin-17 governs hypoxic adaptation of injured epithelium [bulk RNA-seq]

Project description:RORgt deficency impaired wound re-epithelialization. We adopted low-input RNA-seq of purified wound epithelium to explore the underlying epithelial cell functional difference between wild type and RORgt deficient mice during wound healing.

2021-02-18 | GSE166946 | GEO

Aberrant differentiation of epithelial progenitors is accompanied by a hypoxic microenvironment in the paraquat-injured human lung

Project description:Paraquat is a toxic herbicide that can cause severe lung injury, leading to alveolar epithelial cell death, subsequent lung fibrosis and respiratory failure. Understanding the repair process following paraquat injury is critical for developing effective therapeutic strategies to treat paraquat-poisoned patients. However, the lung repair program in paraquat-injured lungs is currently unknown. In this study, we analyzed lung parenchyma samples from an 18-year-old female patient who had ingested paraquat and subsequently underwent a double-lung transplantation on the 34th day after poisoning. By the combination of single cell RNA sequencing analysis and immunostaining analysis, we reveal that the airway stem/progenitor cells and AT2 cells in the paraquat-injured lung exhibit a significantly reduced capacity to regenerate alveolar epithelium epithelial in the paraquat-injured lung. The hypoxic microenvironment may contribute to this aberrant repair program by activating the NOTCH signaling pathway, ultimately leading to an irreversible loss of gas-exchange units and an exacerbated lung tissue damage.

2023-09-28 | GSE231647 | GEO

Bleomycin-injured alveolospheres

Project description:Bleomycin-injured alveolospheres

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