ArticleJournal of cellular biochemistry2021
Increased S1P expression in osteoclasts enhances bone formation in an animal model of Paget's disease.
Article in Journal of cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- Current advances of bone homeostasis imbalance in the cause of hereditary metabolic bone diseases.EFORT open reviews · 2026Review
- Novel aspects of biochemical assessment of bone remodeling and mineralization.Frontiers in endocrinology · 2025Review
- Strategies for the Codelivery of Osteoclasts and Mesenchymal Stem Cells in 3D-Printable Osteochondral Scaffolds.Tissue engineering. Part C, Methods · 2024Article
- Sphingolipid-Induced Bone Regulation and Its Emerging Role in Dysfunction Due to Disease and Infection.International journal of molecular sciences · 2024Review
- The Ying and Yang of Sphingosine-1-Phosphate Signalling within the Bone.International journal of molecular sciences · 2023Review
- Role of Sphingolipids in Multiple Myeloma Progression, Drug Resistance, and Their Potential as Therapeutic Targets.Frontiers in oncology · 2022Review
- Osteoblast Dysfunction in Non-Hereditary Sclerosing Bone Diseases.International journal of molecular sciences · 2021Review
- Increased S1P expression in osteoclasts enhances bone formation in an animal model of Paget's disease.Journal of cellular biochemistry · 2021Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Paget's disease (PD) is characterized by increased numbers of abnormal osteoclasts (OCLs) that drive exuberant bone formation, but the mechanisms responsible for the increased bone formation remain unclear. We previously reported that OCLs from 70% of PD patients express measles virus nucleocapsid protein (MVNP), and that transgenic mice with targeted expression of MVNP in OCLs (MVNP mice) develop bone lesions and abnormal OCLs characteristic of PD. In this report, we examined if OCL-derived sphingosine-1-phosphate (S1P) contributed to the abnormal bone formation in PD, since OCL-derived S1P can act as a coupling factor to increase normal bone formation via binding S1P-receptor-3 (S1PR3) on osteoblasts (OBs). We report that OCLs from MVNP mice and PD patients expressed high levels of sphingosine kinase-1 (SphK-1) compared with wild-type (WT) mouse and normal donor OCLs. SphK-1 production by MVNP-OCLs was interleukin-6 (IL-6)-dependent since OCLs from MVNP/IL-6
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