Regulation of bone formation by osteoclasts involves Wnt/BMP signaling and the chemokine sphingosine-1-phosphate
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Under most conditions, resorbed bone is nearly precisely replaced in location and amount by new bone. Thus, it has long been recognized that bone loss through osteoclast-mediated bone resorption and bone replacement through osteoblast-mediated bone formation are tightly coupled processes. Abundant data conclusively demonstrate that osteoblasts direct osteoclast differentiation. Key questions remain, however, as to how osteoblasts are recruited to the resorption site and how the amount of bone produced is so precisely controlled. We hypothesized that osteoclasts play a crucial role in the promotion of bone formation. We found that osteoclast conditioned medium stimulates human mesenchymal stem (hMS) cell migration and differentiation toward the osteoblast lineage as measured by mineralized nodule formation in vitro. We identified candidate osteoclast-derived coupling factors using the Affymetrix microarray. We observed significant induction of sphingosine kinase 1 (SPHK1), which catalyzes the phosphorylation of sphingosine to form sphingosine 1-phosphate (S1P), in mature multinucleated osteoclasts as compared with preosteoclasts. S1P induces osteoblast precursor recruitment and promotes mature cell survival. Wnt10b and BMP6 also were significantly increased in mature osteoclasts, whereas sclerostin levels decreased during differentiation. Stimulation of hMS cell nodule formation by osteoclast conditioned media was attenuated by the Wnt antagonist Dkk1, a BMP6-neutralizing antibody, and by a S1P antagonist. BMP6 antibodies and the S1P antagonist, but not Dkk1, reduced osteoclast conditioned media-induced hMS chemokinesis. In summary, our findings indicate that osteoclasts may recruit osteoprogenitors to the site of bone remodeling through SIP and BMP6 and stimulate bone formation through increased activation of Wnt/BMP pathways.
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Mature osteoclasts secrete factors that stimulate osteoblast differentiation, including Wnt10b, BMP6, and sphingosine-1-phosphate.
“Furthermore, mature osteoclasts secrete a number of factors that stimulate osteoblast differentiation such as the secreted signaling molecules Wnt10b, BMP6, and the signaling sphingolipid, sphingosine-1-phosphate [180].”
From Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells (2015) · cites this paper as [180]
Several osteoclast-derived factors released into the BRC have been identified and validated in genetically modified mouse models: CT-1, S1P, Wnt10B, BMP6, CTHRC1, C3a, and LIF.
“Several osteoclast-derived factors released into the BRC have been identified and validated in genetically modified mouse models. These factors include cardiotrophin-1 (CT-1),228 S1P,229 Wnt10B, BMP6,230 collagen triple helix repeat-containing 1 (CTHRC1),231 complement factor 3a (C3a),232 and leukemia inhibitory factor (LIF).233”
From Bone remodeling: an operational process ensuring survival and bone mechanical competence (2022) · cites this paper as [230]
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Calcitonin Physiology, Saved by a Lysophospholipid
Martin, T. J., & Sims, N. A. (2015) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.2449 · Cited by 21 · see citing works
Decline in calcitonin receptor expression in osteocytes with age
Gooi, J. H., Chia, L. Y., Walsh, N. C., Karsdal, M. A., Quinn, J. M. W., Martin, T. J., & Sims, N. A. (2014) · Journal of Endocrinology · doi:10.1530/joe-13-0524 · Cited by 22 · see citing works
Tazaki, Y., Sugitani, K., Ogai, K., Kobayashi, I., Kawasaki, H., Aoyama, T., Suzuki, N., Tabuchi, Y., Hattori, A., & Kitamura, K.-I. (2018) · Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology · doi:10.1016/j.cbpa.2018.06.011 · Cited by 15 · see citing works
- Authors
- Pederson, L., Ruan, M., Westendorf, J. J., Khosla, S., & Oursler, M. J.
- Affiliations
- Mayo Clinic (US)
- Endocrine Research Unit,
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2008-12-30
- Volume
- 105
- Issue
- 52
- Pages
- 20764-20769
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2603259
- OpenAlex
- W2058125623
- Cited by
- 556
- References
- 52
- Citations by year
- 2026: 20 · 2025: 16 · 2024: 30 · 2023: 20 · 2022: 38 · 2021: 34 · 2020: 31 · 2019: 45 · 2018: 37 · 2017: 32 · 2016: 24 · 2015: 37 · 2014: 49 · 2013: 45 · 2012: 35
- FWCI
- 8.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Mayo Foundation for Medical Education and Research
- National Institutes of Health
- National Institute on Aging (R01AG028936, AG028936, P01AG004875, AG004875)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Rheumatology › Osteomyelitis and Bone Disorders Research
- Keywords
- bone formation, osteoclasts, bone remodeling, Wnt signaling, BMP signaling, sphingosine-1-phosphate, sphingosine kinase 1, BMP6, Wnt10b, sclerostin, DKK1, mesenchymal stem cells, osteogenic differentiation, chemokinesis, osteoclast recruitment
- MeSH terms
- Sphingosine Kinase, Animals, Calcification, Physiologic, Cell Differentiation, Cell Line, Cell Movement, Humans, Lysophospholipids, Mice, Inbred BALB C, Osteoclasts, Osteogenesis, Proto-Oncogene Proteins, Sphingosine, Signal Transduction, Culture Media, Conditioned, Phosphotransferases (Alcohol Group Acceptor), Chemokines, Intercellular Signaling Peptides and Proteins, Wnt Proteins, Mice, Bone Morphogenetic Protein 6, Mesenchymal Stem Cells
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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