Mouse lung injury-repair induces Ntrk2-tk in CAP1 endothelial cells (scATAC-Seq)
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PROVIDER: PRJNA1085254 | ENA |
REPOSITORIES: ENA
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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
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 | GSE261082 | GEO
Project description:Mouse lung injury-repair induces Ntrk2-tk in CAP1 endothelial cells (scRNA-Seq)
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Project description:Truncated NTRK2 is induced in CAP1 endothelial cells during mouse lung injury-repair
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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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Project description:Role of NTRK2 on ReNcelVM differentiation
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Project description:Independent scientific achievements have led to the discovery of aberrant splicing patterns in oncogenesis while more recent advances have uncovered novel gene fusions involving NTRK2 in gliomas. The exploration of NTRK2 splice variants in normal and neoplastic brain provides an intersection of these two rapidly evolving fields – alternative splicing and NTRK2 involvement in brain tumors. Tropomyosin receptor B (TrkB), encoded by the NTRK2 gene, is known for critical roles in neuronal survival, differentiation, molecular properties associated with memory, and exhibits intricate splicing patterns. Here we show a novel role for a TrkB splice variant, TrkB.T1, in human glioma via NTRK2 transcript analyses and immunostaining using a novel antibody. TrkB.T1 enhances PDGF-driven gliomas in vivo, augments PDGF-induced Akt signaling in vitro, while next generation sequencing broadly implicates TrkB.T1 in the PI3K/Akt signaling cascade in a ligand independent fashion. NTRK2 appears to be a specific example that highlights the importance of expanding upon whole gene and gene fusion analyses to explore splice variants in basic and translational neuro-oncology research
2020-05-13 | GSE136868 | GEO
Project description:RNA was isolated from WT and aSMA-TK wounds at day 6 and day 17 post-wounding
2022-01-10 | GSE178902 | GEO
Project description:Tachykinins (TKs) and their receptors have been shown to be expressed in the mammalian ovary. However, the biological roles for ovarian TKs have yet to be verified. Ci-TK and Ci-TK-R, characterized from the protochordate (ascidian), Ciona intestinalis, are prototypes of vertebrate TKs and their receptors. In the present study, we show a novel biological function of TKs as an inducible factor for oocyte growth using C. intestinalis as a model animal. Immunostaining demonstrated the specific expression of Ci-TK-R in test cells residing in oocytes at the vitellogenic stage. DNA microarray and real-time PCR substantiated that Ci-TK induced gene expression of several proteases including cathepsin D, chymotrypsin, and carboxypeptidase B2 and functionally unidentified lectins or glycosidases in the ovary. The enzymatic activities of the above proteases in the ovary were also shown to be enhanced by Ci-TK. Of particular significance is that treatment of Ciona oocytes with Ci-TK resulted in progression of growth from the vitellogenic stage to the post-vitellogenic stage, which was completely blocked by a TK antagonist or protease inhibitors. These results led to the conclusion that Ci-TK enhances growth of the vitellogenic oocytes via up-regulation of gene expression and enzymatic activities of the proteases. Keywords: tachykinins, ovary
2008-08-19 | GSE8821 | GEO