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Local lung hypoxia determines epithelial fate decisions during alveolar regeneration

ABSTRACT: Local lung hypoxia determines epithelial fate decisions during alveolar regeneration

PROVIDER: PRJNA326204 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3679594_1.fastq.gz	Fastqsanger.gz
	SRR3679594_2.fastq.gz	Fastqsanger.gz
	SRR3679595_1.fastq.gz	Fastqsanger.gz
	SRR3679595_2.fastq.gz	Fastqsanger.gz
	SRR3679596_1.fastq.gz	Fastqsanger.gz

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Local lung hypoxia determines epithelial fate decisions during alveolar regeneration.

Project description:After influenza infection, lineage-negative epithelial progenitors (LNEPs) exhibit a binary response to reconstitute epithelial barriers: activating a Notch-dependent ΔNp63/cytokeratin 5 (Krt5) remodelling program or differentiating into alveolar type II cells (AEC2s). Here we show that local lung hypoxia, through hypoxia-inducible factor (HIF1α), drives Notch signalling and Krt5pos basal-like cell expansion. Single-cell transcriptional profiling of human AEC2s from fibrotic lungs revealed a hypoxic subpopulation with activated Notch, suppressed surfactant protein C (SPC), and transdifferentiation toward a Krt5pos basal-like state. Activated murine Krt5pos LNEPs and diseased human AEC2s upregulate strikingly similar core pathways underlying migration and squamous metaplasia. While robust, HIF1α-driven metaplasia is ultimately inferior to AEC2 reconstitution in restoring normal lung function. HIF1α deletion or enhanced Wnt/β-catenin activity in Sox2pos LNEPs blocks Notch and Krt5 activation, instead promoting rapid AEC2 differentiation and migration and improving the quality of alveolar repair.

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Local lung hypoxia determines epithelial fate decisions during alveolar regeneration

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Mouse pooled LNEPs, pre- and post-influenza - Local lung hypoxia determines epithelial fate decisions during alveolar regeneration

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Klf5 promotes alveolar epithelial type 1 cell lineage commitment during lung development and regeneration

Project description:Alveolar epithelial cell fate decisions drive lung development and regeneration. Using transcriptomic and epigenetic profiling coupled with genetic mouse and organoid models, we identified Klf5 as a critical regulator of alveolar epithelial cell fate across the lifespan. During prenatal lung development and alveologenesis, Klf5 enforces alveolar epithelial type 1 (AT1) cell lineage fidelity. While it is dispensable for both adult AT1 and alveolar epithelial type 2 (AT2) cell homeostasis, Klf5 regulates AT2 cell plasticity after injury. Klf5 represses AT2 cell proliferation and enhances AT2-AT1 cell differentiation in a spatially restricted manner in both infectious and non-infectious models of acute respiratory distress syndrome. Moreover, ex vivo organoid assays reveal that Klf5 modulates AT2 cell fate decisions through reducing AT2 cell sensitivity to inflammatory signaling. These data highlight a major transcriptional regulator of AT1 cell lineage commitment and of the AT2 cell response to inflammatory crosstalk during lung regeneration.

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