ArticleJournal of cellular physiology2019
The effect of Activin-A on periodontal ligament fibroblasts-mediated osteoclast formation in healthy donors and in patients with fibrodysplasia ossificans progressiva.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Periodontium-derived fibroblasts as a model to evaluate inflammation and pharmacological modulation of osteogenesis and osteoclast formation.Frontiers in cell and developmental biology · 2026Review
- Oral biofluid levels of Activin-A and interleukin-1beta in stage III periodontitis.Clinical oral investigations · 2024Article
- SOX2 suppresses osteoblast differentiation of MC3T3-E1 cells through activating the transcription of LGR4.In vitro cellular & developmental biology. Animal · 2023Article
- A Systematic Review of the Evidence of Hematopoietic Stem Cell Differentiation to Fibroblasts.Biomedicines · 2022Review
- Macrophages in heterotopic ossification: from mechanisms to therapy.NPJ Regenerative medicine · 2021Review
- Activin-A Induces Early Differential Gene Expression Exclusively in Periodontal Ligament Fibroblasts fromBiomedicines · 2021Article
- Challenges and Opportunities for Drug Repositioning in Fibrodysplasia Ossificans Progressiva.Biomedicines · 2021Review
- Activin-A Induces Fewer, but Larger Osteoclasts From Monocytes in Both Healthy Controls and Fibrodysplasia Ossificans Progressiva Patients.Frontiers in endocrinology · 2020Article
- Collaboration Around Rare Bone Diseases Leads to the Unique Organizational Incentive of the Amsterdam Bone Center.Frontiers in endocrinology · 2020Article
- Tailored Teaching for Specialized (Para-)medical Students - Experience From Incorporating a Relevant Genetic Disease Throughout a Course of Molecular Cell Biology.Frontiers in public health · 2020Article
- The role of Activin A in fibrodysplasia ossificans progressiva: a prominent mediator.Bioscience reports · 2019Review
- The effect of Activin-A on periodontal ligament fibroblasts-mediated osteoclast formation in healthy donors and in patients with fibrodysplasia ossificans progressiva.Journal of cellular physiology · 2019Article
- The Challenge of Teaching Essential Immunology Laboratory Skills to Undergraduates in One Month-Experience of an Osteoimmunology Course on TLR Activation.Frontiers in immunology · 2019Article
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Authors and funding
8 authors.
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Abstract
Fibrodysplasia ossificans progressiva (FOP) is a genetic disease characterized by heterotopic ossification (HO). The disease is caused by a mutation in the activin receptor type 1 (ACVR1) gene that enhances this receptor's responsiveness to Activin-A. Binding of Activin-A to the mutated ACVR1 receptor induces osteogenic differentiation. Whether Activin-A also affects osteoclast formation in FOP is not known. Therefore we investigated its effect on the osteoclastogenesis-inducing potential of periodontal ligament fibroblasts (PLF) from teeth of healthy controls and patients with FOP. We used western blot analysis of phosphorylated SMAD3 (pSMAD3) and quantitative polymerase chain reaction to assess the effect of Activin-A on the PLF. PLF-induced osteoclast formation and gene expression were studied by coculturing control and FOP PLF with CD14-positive osteoclast precursor cells from healthy donors. Osteoclast formation was also assessed in control CD14 cultures stimulated by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANK-L). Although Activin-A increased activation of the pSMAD3 pathway in both control and FOP PLF, it increased ACVR1, FK binding protein 12 (FKBP12), an inhibitor of DNA binding 1 protein (ID-1) expression only in FOP PLF. Activin-A inhibited PLF mediated osteoclast formation albeit only significantly when induced by FOP PLF. In these cocultures, it reduced M-CSF and dendritic cell-specific transmembrane protein (DC-STAMP) expression. Activin-A also inhibited osteoclast formation in M-CSF and RANK-L mediated monocultures of CD14+ cells by inhibiting their proliferation. This study brings new insight on the role of Activin A in osteoclast formation, which may further add to understanding FOP pathophysiology; in addition to the known Activin-A-mediated HO, this study shows that Activin-A may also inhibit osteoclast formation, thereby further promoting HO formation.
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