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

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

PROVIDER: PRJNA1085248 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR28265020.fastq.gz	Fastqsanger.gz
	SRR28265022.fastq.gz	Fastqsanger.gz
	SRR28265024.fastq.gz	Fastqsanger.gz

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

Project description: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. 

2025-06-20 | GSE261081 | GEO

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

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

Project description:Mouse lung injury-repair induces Ntrk2-tk in CAP1 endothelial cells (scATAC-Seq)

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

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

| PRJNA1085255 | ENA

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

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

2025-06-18 | GSE261083 | GEO

Role of NTRK2 on ReNcelVM differentiation

Project description:The tropomyosin receptor kinase B (TrkB) is encoded by the NTRK2 gene. It belongs to the family of transmembrane tyrosine kinases, which have key roles in the development and maintenance of the nervous system. Brain-derived neurotrophic factor (BDNF) and the neurotrophins NT3 and NT4/5 have high affinity for TrkB. Dysregulation of TrkB is associated to a large spectrum of diseases including neurodegeneration, psychiatric diseases and some cancers. The function of TrkB and its role in neural development have mainly been decrypted using transgenic mouse models, pharmacological modulators and human neuronal cell lines overexpressing NTRK2. In this study, we identified high expression and robust activity of TrkB in ReNcell VM, an immortalized human neural progenitor stem cell line and generated NTRK2-deficient (NTRK2-/-) ReNcell VM using the CRISPR/Cas9 gene editing technology. Global transcriptomic analysis revealed major changes in expression of specific genes responsible for neurogenesis, neuronal development and glial differentiation. In particular, key neurogenic transcription factors were massively down-regulated in NTRK2-/- cells, while early glial progenitor markers were enriched in NTRK2-/- cells. This indicates a previously undescribed inhibitory role of TrkB on glial differentiation in addition to its well described pro-neurogenesis role. Altogether, we have generated for the first time a human neural cell line with a loss-of-function mutation of NTRK2, which represents a reproducible and readily available cell culture system to study the role of TrkB during human neural differentiation, analyse the role of TrkB isoforms as well as validate TrkB antibodies and pharmacological agents targeting the TrkB pathway.

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Role of NTRK2 on ReNcelVM differentiation

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NTRK2 splice variant, TrkB.T1, is the predominant isoform in gliomas and enhances gliomagenesis via PI3K signaling

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