Regulation of osteoclast function and bone mass by RAGE
Open accessAbstract
The receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily that has multiple ligands and is implicated in the pathogenesis of various diseases, including diabetic complications, neurodegenerative disorders, and inflammatory responses. However, the role of RAGE in normal physiology is largely undefined. Here, we present evidence for a role of RAGE in osteoclast maturation and function, which has consequences for bone remodeling. Mice lacking RAGE had increased bone mass and bone mineral density and decreased bone resorptive activity in vivo. In vitro–differentiated RAGE-deficient osteoclasts exhibited disrupted actin ring and sealing zone structures, impaired maturation, and reduced bone resorptive activity. Impaired signaling downstream of αvβ3 integrin was observed in RAGE−/− bone marrow macrophages and precursors of OCs. These results demonstrate a role for RAGE in osteoclast actin cytoskeletal reorganization, adhesion, and function, and suggest that the osteosclerotic-like phenotype observed in RAGE knockout mice is due to a defect in osteoclast function.
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RAGE signaling is known to be important in regulating bone resorption, and mice lacking RAGE have been shown to have increased bone mass and bone mineral density.
“In addition to having a proinflammatory role, however, RAGE signaling is also known to be important in regulating bone resorption, and mice lacking RAGE have been shown to have increased bone mass and bone mineral density (51).”
From Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (2020) · cites this paper as [51]
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References 62 · Cited by 178
- Authors
- Zhou, Z., Immel, D., Xi, C.-X., Bierhaus, A., Feng, X., Mei, L., Nawroth, P., Stern, D. M., & Xiong, W.-C.
- Affiliations
- Augusta University (US)
- Savannah River National Laboratory (US)
- Heidelberg University (DE)
- University of Alabama at Birmingham (US)
- University of Cincinnati (US)
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2006-04-10
- Volume
- 203
- Issue
- 4
- Pages
- 1067-1080
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2118287
- OpenAlex
- W2155953811
- Cited by
- 178
- References
- 62
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 6 · 2023: 8 · 2022: 11 · 2021: 5 · 2020: 10 · 2019: 11 · 2018: 10 · 2017: 10 · 2016: 12 · 2015: 9 · 2014: 6 · 2013: 11 · 2012: 8
- FWCI
- 3.67
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- National Institutes of Health
- U.S. Public Health Service (N40480)
- National Institute of General Medical Sciences (GM 63861, R01GM063861)
- National Institute of Neurological Disorders and Stroke (R01NS045710, R01NS040480, R01NS044521, NS44521, NS045710)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR047830, AR 47830, AR481210, R01AR048120)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Keywords
- receptor for advanced glycation end products, RAGE, osteoclasts, osteoclast maturation, bone remodeling, bone mass, bone mineral density, bone resorption, actin cytoskeleton, sealing zone, integrin αvβ3, bone marrow-derived macrophages, osteosclerosis, RAGE knockout mice
- MeSH terms
- Receptor for Advanced Glycation End Products, Actins, Animals, Bone and Bones, Cell Adhesion, Cell Differentiation, Cells, Cultured, Cytoskeleton, Macrophages, Mice, Inbred C57BL, Osteoclasts, Receptors, Immunologic, Down-Regulation, Macrophage Colony-Stimulating Factor, Glycation End Products, Advanced, Mice, Knockout, Integrin alphaVbeta3, Mice
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