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Mouse lung injury-repair induces Ntrk2-tk in CAP1 endothelial cells (scRNA-Seq)

GSE261082 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/06/20 Platform GPL24247
Summary
The pulmonary capillary endothelial cells (ECs) consist of two populations, CAP1 and CAP2; how each population reacts to diverse tissue injury is incompletely understood. Using single-cell multiome and genetic lineage tracing, we characterize the induction and function of a truncated isoform of Ntrk2, Ntrk2-tk (lacking the tyrosine kinase domain), in multiple lung injury models in mice. Upon Sendai parainfluenza infection, Ntrk2-tk is activated in CAP1 across the whole lung after the initial interferon response, associated with increased intronic accessibility, and persists for weeks after injury. Ntrk2-tk ECs arise from CAP1 but not CAP2, traced by KitCreER and Car4CreER, respectively, and proliferate and give rise to CAP1 but not CAP2, as traced by Ntrk2CreER. EC-specific deletion of Ntrk2 has little molecular and cellular consequences in response to Sendai and H3N2 viral infection. Our data identifies Ntrk2-tk as an EC marker of lung injury-repair and enhances our understanding of EC heterogeneity. 
Published in
Truncated NTRK2 is induced in CAP1 endothelial cells during mouse lung injury-repair
Kong CSL, V M, Pantaleón-García J et al. · iScience 2025 · PMID 40687816 · doi:10.1016/j.isci.2025.112973
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Also filed as BioProject PRJNA1085255 and SRA study SRP494017. Searching any of these in the dataset finder brings you back here.

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