{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:47:01Z","timestamp":1786978021702,"version":"build-2736575974"},"reference-count":58,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2024,5,19]],"date-time":"2024-05-19T00:00:00Z","timestamp":1716076800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2024,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Osteoclasts are the cells primarily responsible for inflammation\u2010induced bone loss, as is particularly seen in rheumatoid arthritis. Increasing evidence suggests that osteoclasts formed under homeostatic versus inflammatory conditions may differ in phenotype. While microRNA\u201029\u20103p family members (miR\u201029a\u20103p, miR\u201029b\u20103p, miR\u201029c\u20103p) promote the function of RANKL\u2010induced osteoclasts, the role of miR\u201029\u20103p during inflammatory TNF\u2010\u03b1\u2010induced osteoclastogenesis is unknown. We used bulk RNA\u2010seq, histology, qRT\u2010PCR, reporter assays, and western blot analysis to examine bone marrow monocytic cell cultures and tissue from male mice in which the function of miR\u201029\u20103p family members was decreased by expression of a miR\u201029\u20103p tough decoy (TuD) competitive inhibitor in the myeloid lineage (LysM\u2010cre). We found that RANKL\u2010treated monocytic cells expressing the miR\u201029\u20103p TuD developed a hypercytokinemia\/proinflammatory gene expression profile in vitro, which is associated with macrophages. These data support the concept that miR\u201029\u20103p suppresses macrophage lineage commitment and may have anti\u2010inflammatory effects. In correlation, when miR\u201029\u20103p activity was decreased, TNF\u2010\u03b1\u2010induced osteoclast formation was accentuated in an in vivo model of localized osteolysis and in a cell\u2010autonomous manner in vitro. Further, miR\u201029\u20103p targets mouse TNF receptor 1 (TNFR1\/\n                    <jats:italic>Tnfrsf1a<\/jats:italic>\n                    ), an evolutionarily conserved regulatory mechanism, which likely contributes to the increased TNF\u2010\u03b1 signaling sensitivity observed in the miR\u201029\u20103p decoy cells. Whereas our previous studies demonstrated that the miR\u201029\u20103p family promotes RANKL\u2010induced bone resorption, the present work shows that miR\u201029\u20103p dampens TNF\u2010\u03b1\u2010induced osteoclastogenesis, indicating that miR\u201029\u20103p has pleiotropic effects in bone homeostasis and inflammatory osteolysis. Our data supports the concept that the knockdown of miR\u201029\u20103p activity could prime myeloid cells to respond to an inflammatory challenge and potentially shift lineage commitment toward macrophage, making the miR\u201029\u20103p family a potential therapeutic target for modulating inflammatory response.\n                  <\/jats:p>","DOI":"10.1002\/jcp.31299","type":"journal-article","created":{"date-parts":[[2024,5,20]],"date-time":"2024-05-20T01:25:56Z","timestamp":1716168356000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["The miR\u201029\u20103p family suppresses inflammatory osteolysis"],"prefix":"10.1002","volume":"239","author":[{"given":"Bongjin","family":"Shin","sequence":"first","affiliation":[{"name":"Center on Aging, UConn Health Farmington Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henry 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