Cited by 135Bone Metabolism and DiseasesBone health and osteoporosis researchTelomeres, Telomerase, and Senescence

DNA damage drives accelerated bone aging via an NF- κ B–dependent mechanism

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Chen, Qian, Liu, Kai, Robinson, Andria R, Clauson, Cheryl L, Blair, Harry C, Robbins, Paul D, Niedernhofer, Laura J, Ouyang, Hongjiao·2013·Journal of Bone and Mineral Research

Abstract

Advanced age is one of the most important risk factors for osteoporosis. Accumulation of oxidative DNA damage has been proposed to contribute to age-related deregulation of osteoblastic and osteoclastic cells. Excision repair cross complementary group 1–xeroderma pigmentosum group F (ERCC1-XPF) is an evolutionarily conserved structure-specific endonuclease that is required for multiple DNA repair pathways. Inherited mutations affecting expression of ERCC1-XPF cause a severe progeroid syndrome in humans, including early onset of osteopenia and osteoporosis, or anomalies in skeletal development. Herein, we used progeroid ERCC1-XPF–deficient mice, including Ercc1-null (Ercc1−/−) and hypomorphic (Ercc1−/Δ) mice, to investigate the mechanism by which DNA damage leads to accelerated bone aging. Compared to their wild-type littermates, both Ercc1−/− and Ercc1−/Δ mice display severe, progressive osteoporosis caused by reduced bone formation and enhanced osteoclastogenesis. ERCC1 deficiency leads to atrophy of osteoblastic progenitors in the bone marrow stromal cell (BMSC) population. There is increased cellular senescence of BMSCs and osteoblastic cells, as characterized by reduced proliferation, accumulation of DNA damage, and a senescence-associated secretory phenotype (SASP). This leads to enhanced secretion of inflammatory cytokines known to drive osteoclastogenesis, such as interleukin-6 (IL-6), tumor necrosis factor α (TNFα), and receptor activator of NF-κB ligand (RANKL), and thereby induces an inflammatory bone microenvironment favoring osteoclastogenesis. Furthermore, we found that the transcription factor NF-κB is activated in osteoblastic and osteoclastic cells of the Ercc1 mutant mice. Importantly, we demonstrated that haploinsufficiency of the p65 NF-κB subunit partially rescued the osteoporosis phenotype of Ercc1−/Δ mice. Finally, pharmacological inhibition of the NF-κB signaling via an I-κB kinase (IKK) inhibitor reversed cellular senescence and SASP in Ercc1−/Δ BMSCs. These results demonstrate that DNA damage drives osteoporosis through an NF-κB–dependent mechanism. Therefore, the NF-κB pathway represents a novel therapeutic target to treat aging-related bone disease. © 2013 American Society for Bone and Mineral Research.

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  • NF-κB activation has been observed in numerous diseases associated with aging, including sarcopenia, osteoporosis, and neurodegenerative diseases.

    “NF-κB activation has been observed in numerous diseases associated with aging (91), including sarcopenia (92), osteoporosis (93), and neurodegenerative diseases (94).”

    From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [93]

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  1. [17]Miyamoto S 2011 Nuclear initiated NF-[kappa]B signaling: NEMO and ATM take center stage Cell Res 21 1 116 130 21187855 PMC3193401
  2. [49]Chang J Wang Z Tang E Fan Z McCauley L Franceschi R Guan K Krebsbach PH Wang C-Y 2009 Inhibition of osteoblastic bone formation by nuclear factor-[kappa]B Nat Med 15 6 682 689 19448637 PMC2768554

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Authors
Chen, Q., Liu, K., Robinson, A. R., Clauson, C. L., Blair, H. C., Robbins, P. D., Niedernhofer, L. J., & Ouyang, H.
Affiliations
University of Pittsburgh (US)
Corresponding author
Ouyang, Hongjiao
Venue
Journal of Bone and Mineral Research
Published
2012-12-21
Volume
28
Issue
5
Pages
1214-1228
ISSN
  • 0884-0431 (ISSN-L)
  • 1523-4681
OpenAlex
W2052845629
Cited by
135
References
52
Citations by year
2026: 12 · 2025: 10 · 2024: 16 · 2023: 12 · 2022: 9 · 2021: 16 · 2020: 5 · 2019: 13 · 2018: 8 · 2017: 5 · 2016: 9 · 2015: 8 · 2014: 7 · 2013: 5
FWCI
2.57
Type
journal article
Language
en
Open access
Locations
  • Journal of Bone and Mineral Research (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • U.S. Department of Veterans Affairs
  • Ellison Medical Foundation (P30CA047904, AG-NS-0303-05, P30AG024827, ES016114)
  • Multiple Myeloma Research Foundation
  • Scoliosis Research Society
  • University of Pittsburgh (P30-AG024827, P30 CA047904)
  • National Institutes of Health (AG-NS-0303-05, AG024827)
  • VA Pittsburgh Healthcare System
  • National Institute on Aging (R21AG033907, AG 024827, AG033907, P30AG024827)
  • National Cancer Institute (ES016114, R21CA161150, P30CA047904)
  • National Institute of Neurological Disorders and Stroke (U01NS058451, NS058451)
  • National Institute of Environmental Health Sciences (ES 016114, R01ES016114)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR051456, R01AR055208, R01AR051456)
  • National Institute of Dental and Craniofacial Research (R01DE017439)
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 › Physiology › Telomeres, Telomerase, and Senescence
Keywords
DNA damage, bone aging, osteoporosis, NF-κB signaling, ERCC1, progeroid syndromes, cellular senescence, senescence-associated secretory phenotype, mesenchymal stem cells, osteoclastogenesis, bone formation, IKK inhibitor, NF-κB p65, inflammatory cytokines, RANKL
MeSH terms
Animals, Bone and Bones, Cell Differentiation, Cells, Cultured, DNA Damage, DNA-Binding Proteins, Endonucleases, Osteoblasts, Osteoporosis, NF-kappa B, Mice, Knockout, Mice

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