ArticleThe Journal of biological chemistry2014
Fibrodysplasia ossificans progressiva-related activated activin-like kinase signaling enhances osteoclast formation during heterotopic ossification in muscle tissues.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Case Report: Unusual Heterotopic Ossification of the Hindfoot.Frontiers in surgery · 2022Article
- MyD88 Is Not Required for Muscle Injury-Induced Endochondral Heterotopic Ossification in a Mouse Model of Fibrodysplasia Ossificans Progressiva.Biomedicines · 2021Article
- Effects of fluid flow shear stress to mouse muscle cells on the bone actions of muscle cell-derived extracellular vesicless.PloS one · 2021Article
- Prognostic Value of Bone Formation and Resorption Proteins in Heterotopic Ossification in Critically-Ill Patients. a Single-Centre Study.Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) · 2021Article
- When the Nervous System Turns Skeletal Muscles into Bones: How to Solve the Conundrum of Neurogenic Heterotopic Ossification.Current osteoporosis reports · 2020Review
- Article
- Roles of Dkk2 in the Linkage from Muscle to Bone during Mechanical Unloading in Mice.International journal of molecular sciences · 2020Article
- Bioinformatics Analysis of the Molecular Mechanism of Late-Stage Heterotopic Ossification.BioMed research international · 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
- Heterotopic Ossification: A Comprehensive Review.JBMR plus · 2019Review
- Smad-dependent mechanisms of inflammatory bone destruction.Arthritis research & therapy · 2016Review
- Role of osteoclasts in heterotopic ossification enhanced by fibrodysplasia ossificans progressiva-related activin-like kinase 2 mutation in mice.Journal of bone and mineral metabolism · 2016Article
- The biological function of type I receptors of bone morphogenetic protein in bone.Bone research · 2016Review
- Trauma-induced heterotopic bone formation and the role of the immune system: A review.The journal of trauma and acute care surgery · 2016Review
- ACVR1R206H receptor mutation causes fibrodysplasia ossificans progressiva by imparting responsiveness to activin A.Science translational medicine · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrodysplasia ossificans progressiva is characterized by extensive ossification within muscle tissues, and its molecular pathogenesis is responsible for the constitutively activating mutation (R206H) of the bone morphogenetic protein type 1 receptor, activin-like kinase 2 (ALK2). In this study, we investigated the effects of implanting ALK2 (R206H)-transfected myoblastic C2C12 cells into nude mice on osteoclast formation during heterotopic ossification in muscle and subcutaneous tissues. The implantation of ALK2 (R206H)-transfected C2C12 cells with BMP-2 in nude mice induced robust heterotopic ossification with an increase in the formation of osteoclasts in muscle tissues but not in subcutaneous tissues. The implantation of ALK2 (R206H)-transfected C2C12 cells in muscle induced heterotopic ossification more effectively than that of empty vector-transfected cells. A co-culture of ALK2 (R206H)-transfected C2C12 cells as well as the conditioned medium from ALK2 (R206H)-transfected C2C12 cells enhanced osteoclast formation in Raw264.7 cells more effectively than those with empty vector-transfected cells. The transfection of ALK2 (R206H) into C2C12 cells elevated the expression of transforming growth factor (TGF)-β, whereas the inhibition of TGF-β signaling suppressed the enhanced formation of osteoclasts in the co-culture with ALK2 (R206H)-transfected C2C12 cells and their conditioned medium. In conclusion, this study demonstrated that the causal mutation transfection of fibrodysplasia ossificans progressiva in myoblasts enhanced the formation of osteoclasts from its precursor through TGF-β in muscle tissues.
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