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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

ADAM-10 Is Involved in Osteoblast Mineralization and Rheumatoid Arthritis-Associated Bone Destruction

  • Haruka Nakamura1
  • Hiroyuki Kojima1
  • Kohei Maeda1
  • Kosuke Sakurai1
  • Toshihiro Tanioka1
  • Sho Ishii2
  • Kuninobu Wakabayashi2
  • Masahiro Hosonuma3,4
  • Yuki Azetsu4,5
  • Masayuki Iyoda6,7
  • Masamichi Takami4,5
  • Takeo Isozaki1,2
7 affiliations
  1. 1Department of Pathogenesis and Translational Medicine, Showa Medical University Graduate School of Pharmacy, Tokyo 142-8555, Japan
  2. 2Division of Rheumatology, Department of Medicine, Showa Medical University, Tokyo 142-8555, Japan
  3. 3Division of Medical Pharmacology, Department of Pharmacology, Showa Medical University School of Medicine, Tokyo 142-8555, Japan
  4. 4Pharmacological Research Center, Showa Medical University, Tokyo 142-8555, Japan
  5. 5Department of Pharmacology, Graduate School of Dentistry, Showa Medical University, Tokyo 142-8555, Japan
  6. 6Department of Microbiology and Immunology, Showa Medical University Graduate School of Medicine, Tokyo 142-8555, Japan
  7. 7Division of Nephrology, Department of Medicine, Showa Medical University Graduate School of Medicine, Tokyo 142-8555, Japan
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Abstract

Rheumatoid arthritis (RA), a chronic autoimmune condition, causes irreversible bone destruction. A disintegrin and metalloprotease 10 (ADAM-10) has been implicated in inflammatory processes in RA. We investigated the potential role of ADAM-10 in osteoblast mineralization and RA-associated bone destruction. Serum ADAM-10 levels in RA patients were measured by ELISA, and ADAM-10 expression in osteoblasts was assessed by Western blotting. Collagen-induced arthritis (CIA) mice were treated intraperitoneally with the ADAM-10 inhibitor GI254023X (100 mg/kg) for three weeks. Arthritis and bone destruction were evaluated by macroscopic, immunohistochemical, histological, and micro-CT analyses. The effects of ADAM-10 inhibition on primary osteoblast mineralization were also assessed by Alizarin Red S staining. Serum ADAM-10 levels in patients with RA tended to be higher at Stage III of the Steinbrocker classification. In CIA mice, ADAM-10 inhibition attenuated weight loss, paw swelling, and arthritis scores and suppressed bone destruction. ADAM-10 inhibition also significantly reduced Rankl expression in knee joints. Furthermore, the inhibition reversed the suppression of primary osteoblast mineralization induced by TNF-α. Pharmacological inhibition of ADAM-10 attenuated experimental arthritis and bone destruction and improved osteoblast mineralization, suggesting that ADAM-10 may contribute to inflammatory bone destruction in RA.

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Cite

BibTeXRIS
BibTeX
@article{nakamura2026adam10,
  title = {{ADAM-10 Is Involved in Osteoblast Mineralization and Rheumatoid Arthritis-Associated Bone Destruction}},
  author = {Haruka Nakamura and Hiroyuki Kojima and Kohei Maeda and Kosuke Sakurai and Toshihiro Tanioka and Sho Ishii and Kuninobu Wakabayashi and Masahiro Hosonuma and Yuki Azetsu and Masayuki Iyoda and Masamichi Takami and Takeo Isozaki},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = nov,
  doi = {10.3390/ijms27219842},
  url = {https://www.mdpi.com/1422-0067/27/21/9842},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - ADAM-10 Is Involved in Osteoblast Mineralization and Rheumatoid Arthritis-Associated Bone Destruction
AU  - Haruka Nakamura
AU  - Hiroyuki Kojima
AU  - Kohei Maeda
AU  - Kosuke Sakurai
AU  - Toshihiro Tanioka
AU  - Sho Ishii
AU  - Kuninobu Wakabayashi
AU  - Masahiro Hosonuma
AU  - Yuki Azetsu
AU  - Masayuki Iyoda
AU  - Masamichi Takami
AU  - Takeo Isozaki
PY  - 2026
DA  - 2026/11/03
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27219842
UR  - https://www.mdpi.com/1422-0067/27/21/9842
AB  - Rheumatoid arthritis (RA), a chronic autoimmune condition, causes irreversible bone destruction. A disintegrin and metalloprotease 10 (ADAM-10) has been implicated in inflammatory processes in RA. We investigated the potential role of ADAM-10 in osteoblast mineralization and RA-associated bone destruction. Serum ADAM-10 levels in RA patients were measured by ELISA, and ADAM-10 expression in osteoblasts was assessed by Western blotting. Collagen-induced arthritis (CIA) mice were treated intraperitoneally with the ADAM-10 inhibitor GI254023X (100 mg/kg) for three weeks. Arthritis and bone destruction were evaluated by macroscopic, immunohistochemical, histological, and micro-CT analyses. The effects of ADAM-10 inhibition on primary osteoblast mineralization were also assessed by Alizarin Red S staining. Serum ADAM-10 levels in patients with RA tended to be higher at Stage III of the Steinbrocker classification. In CIA mice, ADAM-10 inhibition attenuated weight loss, paw swelling, and arthritis scores and suppressed bone destruction. ADAM-10 inhibition also significantly reduced Rankl expression in knee joints. Furthermore, the inhibition reversed the suppression of primary osteoblast mineralization induced by TNF-α. Pharmacological inhibition of ADAM-10 attenuated experimental arthritis and bone destruction and improved osteoblast mineralization, suggesting that ADAM-10 may contribute to inflammatory bone destruction in RA.
SN  - 1422-0067
ER  -