ArticleJournal of cellular and molecular medicine2019
Neurotrophin-3 acts on the endothelial-mesenchymal transition of heterotopic ossification in rats.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 23 citations in OpenAlex.
- Neurogenic heterotopic ossification: from molecular mechanisms to clinical treatment.Journal of orthopaedic translation · 2026Review
- M2 macrophages promote heterotopic ossification through MSX2 binding to LEF1-mediated endothelial-mesenchymal transition.Stem cell research & therapy · 2026Article
- Deciphering the Regulatory Networks of the Migrasome-Associated Cell Subpopulation in Heterotopic Ossification via Multi-Omics Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Heterotopic ossification: Current developments and emerging potential therapies.Chinese medical journal · 2025Review
- A Procedural Overview of the Involvement of Small Molecules in the Nervous System in the Regulation of Bone Healing.International journal of nanomedicine · 2025Review
- TrkC protects against osteoarthritis progression by maintaining articular cartilage homeostasis.International journal of biological sciences · 2025Article
- Mast cell activation by NGF drives the formation of trauma-induced heterotopic ossification.JCI insight · 2024Article
- The Role of Neuromodulation and Potential Mechanism in Regulating Heterotopic Ossification.Neurochemical research · 2024Review
- Multi-tissue transcriptomics of a unique monozygotic discordant twin case of severe progressive osseous heteroplasia.Genes & diseases · 2024Article
- Roles of Plasminogen Activator Inhibitor-1 in Heterotopic Ossification Induced by Achilles Tenotomy in Thermal Injured Mice.Calcified tissue international · 2024Article
- Neurovascular Interactions in the Development of the Vasculature.Life (Basel, Switzerland) · 2022Review
- Nervous System-Driven Osseointegration.International journal of molecular sciences · 2022Review
- Contemporary perspectives on heterotopic ossification.JCI insight · 2022Review
- Capacitive interdigitated system of high osteoinductive/conductive performance for personalized acting-sensing implants.NPJ Regenerative medicine · 2021Article
- Macrophages in heterotopic ossification: from mechanisms to therapy.NPJ Regenerative medicine · 2021Review
- Neuromodulation of bone: Role of different peptides and their interactions (Review).Molecular medicine reports · 2021Review
- Quercetin Attenuates Trauma-Induced Heterotopic Ossification by Tuning Immune Cell Infiltration and Related Inflammatory Insult.Frontiers in immunology · 2021Article
- Melatonin Promotes Heterotopic Ossification Through Regulation of Endothelial-Mesenchymal Transition in Injured Achilles Tendons in Rats.Frontiers in cell and developmental biology · 2021Article
- Macrophage-derived neurotrophin-3 promotes heterotopic ossification in rats.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Endothelial to mesenchymal transition contributes to nicotine-induced atherosclerosis.Theranostics · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the fact that extensive studies have focused on heterotopic ossification (HO), its molecular mechanism remains unclear. The endothelial-mesenchymal transition (EndMT), which may be partially modulated by neuroendocrine cytokines is thought to play a major role in HO. Neurotrophin-3 (NT-3), which has neuroendocrine characteristics is believed to promote skeletal remodeling. Herein, we suggest that that NT-3 may promote HO formation through regulation of EndMT. Here, we used an in vivo model of HO and an in vitro model of EndMT induction to elucidate the effect and underlying mechanism of NT-3 on EndMT in HO. Our results showed that heterotopic bone and cartilage arose from EndMT and NT-3 promoted HO formation in vivo. Our in vitro results showed that NT-3 up-regulated mesenchymal markers (FSP-1, α-SMA and N-cadherin) and mesenchymal stem cell (MSC) markers (STRO-1, CD44 and CD90) and down-regulated endothelial markers (Tie-1, VE-cadherin and CD31). Moreover, NT-3 enhanced a chondrogenesis marker (Sox9) and osteogenesis markers (OCN and Runx2) via activation of EndMT. However, both EndMT specific inhibitor and tropomyosin-related kinase C (TrkC) specific inhibitor rescued NT-3-induced HO formation and EndMT induction in vivo and in vitro. In conclusion, our findings demonstrate that NT-3 promotes HO formation via modulation of EndMT both in vivo and in vitro, which offers a new potential target for the prevention and therapy of HO.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.