Chloroquine reduces osteoclastogenesis in murine osteoporosis by preventing TRAF3 degradation
Open accessAbstract
The cytokines RANKL and TNF activate NF-κB signaling in osteoclast precursors (OCPs) to induce osteoclast (OC) formation. Conversely, TNF can limit OC formation through NF-κB p100, which acts as an inhibitor, and TNF receptor-associated receptor 3 (TRAF3); however, a role for TRAF3 in RANKL-mediated OC formation is unknown. We found that TRAF3 limits RANKL-induced osteoclastogenesis by suppressing canonical and noncanonical NF-κB signaling. Conditional OC-specific Traf3-KO (cKO) mice had mild osteoporosis and increased OC formation. RANKL induced TRAF3 degradation via the lysosome/autophagy system. The autophagy/lysosome inhibitor chloroquine reduced RANKL-induced OC formation and function by increasing TRAF3 expression in OCPs in vitro and in vivo. Although chloroquine had no effect on basal bone resorption, it inhibited parathyroid hormone- and ovariectomy-induced OC activation in WT, but not cKO, mice. Deletion of the transcription factor gene Relb resulted in increased TRAF3 expression in OCPs, which was associated with decreased RANKL-induced TRAF3 degradation. RelB directly increased expression of BECN1, a key autophagy regulator, by binding to its promoter. These data indicate that autophagic/lysosomal degradation of TRAF3 is an important step in RANKL-induced NF-κB activation in OCPs. Furthermore, treatments that increase TRAF3 levels in OCPs, including pharmacological inhibition of its degradation with compounds such as chloroquine, may limit bone destruction in common bone diseases.
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Conditional deletion of TRAF3, an inhibitor of the noncanonical pathway, in osteoclast precursors resulted in increased osteoclast formation and bone resorption in mice.
“conditional deletion of TRAF3, an inhibitor of the noncanonical pathway, in osteoclast precursors resulted in increased osteoclast formation and bone resorption in mice.171”
From Bone remodeling: an operational process ensuring survival and bone mechanical competence (2022) · cites this paper as [171]
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- Authors
- Xiu, Y., Xu, H., Zhao, C., Li, J., Morita, Y., Yao, Z., Xing, L., & Boyce, B. F.
- Affiliations
- University of Rochester Medicine (US)
- Corresponding author
- Boyce, Brendan F.
- Venue
- Journal of Clinical Investigation
- Published
- 2013-12-09
- Volume
- 124
- Issue
- 1
- Pages
- 297-310
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3871219
- OpenAlex
- W2103768376
- Cited by
- 164
- References
- 72
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 7 · 2023: 12 · 2022: 14 · 2021: 16 · 2020: 26 · 2019: 20 · 2018: 13 · 2017: 20 · 2016: 6 · 2015: 7 · 2014: 4
- FWCI
- 2.54
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Rochester
- Medical Center, University of Rochester
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (P30AR061307, T32AR053459, AR 43510, AR 48697, R01AR048697, R01AR063650, R01AR043510)
- National Center for Research Resources (S10RR027340)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Keywords
- chloroquine, osteoclastogenesis, TRAF3, RANKL, NF-κB signaling, autophagy, lysosomal degradation, osteoporosis, RelB, Beclin-1, osteoclast precursors, bone resorption, ovariectomy, parathyroid hormone
- MeSH terms
- Beclin-1, Animals, Bone Resorption, Cells, Cultured, Chloroquine, Female, Gene Expression Regulation, Lysosomes, Mice, Inbred C57BL, Osteoclasts, Osteoporosis, Promoter Regions, Genetic, Protein Binding, Mice, Knockout, TNF Receptor-Associated Factor 3, Apoptosis Regulatory Proteins, Mice, Transcription Factor RelB, RANK Ligand, Proteolysis
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