ArticleJournal of visualized experiments : JoVE2018
A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation.
Article in Journal of visualized experiments : JoVE, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Identification of anti-resorptive GPCRs by high-content imaging in human osteoclasts.Journal of molecular endocrinology · 2025Article
- The NaJournal of extracellular vesicles · 2024Article
- Yunnan Baiyao Inhibits Periodontitis by Suppressing the Autophagic Flux.International dental journal · 2024Article
- 3'-Sialyllactose alleviates bone loss by regulating bone homeostasis.Communications biology · 2024Article
- Dual Role of Interleukin-20 in Different Stages of Osteoclast Differentiation and Its Osteoimmune Regulation during Alveolar Bone Remodeling.International journal of molecular sciences · 2023Article
- Biological Evaluation and Transcriptomic Analysis of Corylin as an Inhibitor of Osteoclast Differentiation.International journal of molecular sciences · 2021Article
- Inhibitory Effects of Gold and Silver Nanoparticles on the Differentiation into Osteoclasts In Vitro.Pharmaceutics · 2021Article
- Rapamycin could increase the effects of melatonin against age-dependent bone loss.Zeitschrift fur Gerontologie und Geriatrie · 2020Article
- Kaempferol promotes bone formation in part via the mTOR signaling pathway.Molecular medicine reports · 2019Article
- Macrophage colony-stimulating factor pretreatment of bone marrow progenitor cells regulates osteoclast differentiation based upon the stage of myeloid development.Journal of cellular biochemistry · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoclasts are unique bone-resorbing cells that differentiate from the monocyte/macrophage lineage of bone marrow. Dysfunction of osteoclasts may result in a series of bone metabolic diseases, including osteoporosis. To develop pharmaceutical targets for the prevention of pathological bone mass loss, the mechanisms by which osteoclasts differentiate from precursors must be understood. The ability to isolate and culture a large number of osteoclasts in vitro is critical in order to determine the role of specific genes in osteoclast differentiation. Inactivation of the mammalian/mechanistic target of rapamycin complex 1 (TORC1) in osteoclasts can decrease osteoclast number and increase bone mass; however, the underlying mechanisms require further study. In the present study, a RANKL-based protocol to isolate and culture osteoclasts from mouse bone marrow and to study the influence of mTORC1 inactivation on osteoclast formation is described. This protocol successfully resulted in a large number of giant osteoclasts, typically within one week. Deletion of Raptor impaired osteoclast formation and decreased the activity of secretory tartrate-resistant acid phosphatase, indicating that mTORC1 is critical for osteoclast formation.
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Registered trials
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