ArticleInternational journal of molecular sciences2019
Overexpression of Notch Signaling Induces Hyperosteogeny in Zebrafish.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Myeloid-Specific Deletion ofBiomedicines · 2026Article
- Spatiotemporal application of small molecules in fracture healing.Biomaterials translational · 2025Review
- Signaling network regulating osteogenesis in mesenchymal stem cells.Journal of cell communication and signaling · 2022Review
- Metabolomics in Bone Research.Metabolites · 2021Review
- Weak genetic signal for phenotypic integration implicates developmental processes as major regulators of trait covariation.Molecular ecology · 2021Article
- Zebrafish: A Resourceful Vertebrate Model to Investigate Skeletal Disorders.Frontiers in endocrinology · 2020Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Notch signaling is one of the evolutionarily conserved signaling pathways in multicellular organisms. It plays an important role in embryonic development. During skeletal development of vertebrates, it regulates bone homeostasis by manipulating both osteoblastogenesis and osteoclastogenesis through different mechanisms. However, due to the different nature of Notch signaling in mesenchymal stem cell and osteoblast, regulation of Notch signaling in bone-related diseases remains unsettled. Previous studies by cell culture and mouse models showed contradictory results regarding the role of Notch signaling in bone homeostasis. To clarify the role of Notch signaling in osteogenesis, we established a zebrafish model, in which Notch1a intracellular domain (N1aICD) was specifically expressed in the osteoblasts. We found that overexpression of N1aICD in osteoblasts caused hyperosteogeny in the column region of zebrafish with the morphology of narrowed neural/hemal canals. Moreover, increased metabolic activity of osteoblasts instead of augmenting osteoblast number led to hyperosteogeny in N1aICD-overexpressed zebrafish. In summary, we successfully established a transgenic zebrafish line overexpressing N1aICD to clarify the in-vivo function of Notch signaling during osteoblastogenesis. In the future, this fish line can serve as a valuable tool to test the therapeutic drugs for hyperosteogeny.
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Registered trials
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