{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T07:22:02Z","timestamp":1793863322156,"version":"4.6.1"},"reference-count":52,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2024,1,27]],"date-time":"2024-01-27T00:00:00Z","timestamp":1706313600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"Japan Society for the Promotion of Science (JSPS) KAKENHI","award":["JP23689066"],"award-info":[{"award-number":["JP23689066"]}]},{"name":"Japan Society for the Promotion of Science (JSPS) KAKENHI","award":["JP17K19728"],"award-info":[{"award-number":["JP17K19728"]}]},{"name":"Japan Society for the Promotion of Science (JSPS) KAKENHI","award":["JP19H03786"],"award-info":[{"award-number":["JP19H03786"]}]},{"name":"Japan Society for the Promotion of Science (JSPS) KAKENHI","award":["JP22H03203"],"award-info":[{"award-number":["JP22H03203"]}]},{"name":"Chugai Foundation for Innovative Drug Discovery Science: C-FINDs"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,4,19]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by synovitis, bone and cartilage destruction, and increased fracture risk with bone loss. Although disease\u2013modifying antirheumatic drugs have dramatically improved clinical outcomes, these therapies are not universally effective in all patients because of the heterogeneity of RA pathogenesis. Therefore, it is necessary to elucidate the molecular mechanisms underlying RA pathogenesis, including associated bone loss, in order to identify novel therapeutic targets. In this study, we found that Budding uninhibited by benzimidazoles 1 (BUB1) was highly expressed in RA patients\u2019 synovium and murine ankle tissue with arthritis. As CD45+CD11b+ myeloid cells are a Bub1 highly expressing population among synovial cells in mice, myeloid cell\u2013specific Bub1 conditional knockout (Bub1\u0394LysM) mice were generated. Bub1\u0394LysM mice exhibited reduced femoral bone mineral density when compared with control (Ctrl) mice under K\/BxN serum\u2013transfer arthritis, with no significant differences in joint inflammation or bone erosion based on a semi\u2013quantitative erosion score and histological analysis. Bone histomorphometry revealed that femoral bone mass of Bub1\u0394LysM under arthritis was reduced by increased osteoclastic bone resorption. RNA-seq and subsequent Gene Set Enrichment Analysis demonstrated a significantly enriched nuclear factor-kappa B pathway among upregulated genes in receptor activator of nuclear factor kappa B ligand (RANKL)\u2013stimulated bone marrow\u2013derived macrophages (BMMs) obtained from Bub1\u0394LysM mice. Indeed, osteoclastogenesis using BMMs derived from Bub1\u0394LysM was enhanced by RANKL and tumor necrosis factor-\u03b1 or RANKL and IL-1\u03b2 treatment compared with Ctrl. Finally, osteoclastogenesis was increased by Bub1 inhibitor BAY1816032 treatment in BMMs derived from wildtype mice. These data suggest that Bub1 expressed in macrophages plays a protective role against inflammatory arthritis\u2013associated bone loss through inhibition of inflammation\u2013mediated osteoclastogenesis.<\/jats:p>","DOI":"10.1093\/jbmr\/zjae015","type":"journal-article","created":{"date-parts":[[2024,1,24]],"date-time":"2024-01-24T07:33:56Z","timestamp":1706081636000},"page":"341-356","source":"Crossref","is-referenced-by-count":15,"title":["Bub1 suppresses inflammatory arthritis\u2013associated bone loss in mice through inhibition of TNF\u03b1\u2013mediated osteoclastogenesis"],"prefix":"10.1093","volume":"39","author":[{"given":"Shuhei","family":"Yoshida","sequence":"first","affiliation":[{"name":"Department of Pathophysiology, Ehime University Graduate School of Medicine , Toon, Ehime, 791-0295 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aoi","family":"Ikedo","sequence":"additional","affiliation":[{"name":"Division of Integrative Pathophysiology , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"},{"name":"Ehime University , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuta","family":"Yanagihara","sequence":"additional","affiliation":[{"name":"Division of Integrative Pathophysiology , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"},{"name":"Ehime University , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomohisa","family":"Sakaue","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine , Toon, Ehime, 791-0295 , Japan"},{"name":"Division of Cell Growth and Tumor Regulation , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"},{"name":"Ehime University , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noritaka","family":"Saeki","sequence":"additional","affiliation":[{"name":"Division of Integrative Pathophysiology , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"},{"name":"Ehime University , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"},{"name":"Division of Medical Research Support , Advanced Research Support Center, , Toon, Ehime, 791-0295 , Japan"},{"name":"Ehime University , Advanced Research Support Center, , Toon, Ehime, 791-0295 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuuki","family":"Imai","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology, Ehime University Graduate School of Medicine , Toon, Ehime, 791-0295 , Japan"},{"name":"Division of Integrative Pathophysiology , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"},{"name":"Ehime University , Proteo-Science Center (PROS), , Toon, Ehime, 791-0295 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,1,27]]},"reference":[{"issue":"12","key":"2024041923104117700_ref1","first-page":"2255","article-title":"The pathogenesis of rheumatoid arthritis","volume":"55","author":"McInnes","year":"2011","journal-title":"N Engl J Med"},{"issue":"3","key":"2024041923104117700_ref2","doi-asserted-by":"crossref","first-page":"522","DOI":"10.1002\/1529-0131(200003)43:3<522::AID-ANR7>3.0.CO;2-Y","article-title":"Bone mineral density and frequency of osteoporosis in female patients with rheumatoid arthritis: results from 394 patients in the Oslo County rheumatoid arthritis register","volume":"43","author":"Haugeberg","year":"2000","journal-title":"Arthritis Rheum"},{"issue":"8","key":"2024041923104117700_ref3","doi-asserted-by":"crossref","first-page":"1680","DOI":"10.3899\/jrheum.101196","article-title":"Arthritis increases the risk for fractures \u2014 results from the women\u2019s 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