Mouse lung injury-repair induces Ntrk2-tk in CAP1 endothelial cells (scATAC-Seq)
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ABSTRACT: 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.
ORGANISM(S): Mus musculus
PROVIDER: GSE261081 | GEO | 2025/06/20
REPOSITORIES: GEO
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