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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE166948 | GEO | 2021/02/18

REPOSITORIES: GEO

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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.

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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.

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Interleukin-17 governs hypoxic adaptation of injured epithelium

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

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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.

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

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

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Interleukin-17 governs hypoxic adaptation of injured epithelium

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

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

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