Truncated NTRK2 is induced in CAP1 endothelial cells during mouse lung injury-repair.

ABSTRACT: 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 mouse genetics, we characterize the induction and function of a truncated isoform of Ntrk2, Ntrk2-T1, in multiple lung injury models. Upon Sendai parainfluenza infection, Ntrk2-T1 is broadly induced in CAP1s after the initial interferon response, associated with increased intronic chromatin accessibility, and persists for weeks. Ntrk2-T1 ECs arise from CAP1s but not CAP2s-traced by Kit ^CreER and Car4 ^CreER , respectively-and proliferate and give rise to CAP1s but not CAP2s, as traced by Ntrk2 ^CreER . Although also induced

SUBMITTER: Kong CSL 

PROVIDER: S-EPMC12275058 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature