{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T18:50:00Z","timestamp":1790621400198,"version":"4.1.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2016,6,1]],"date-time":"2016-06-01T00:00:00Z","timestamp":1464739200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Increased osteoclastogenesis is responsible for osteolysis, which is a severe consequence of inflammatory diseases associated with bone destruction, such as rheumatoid arthritis and periodontitis. The mechanisms that limit osteoclastogenesis under inflammatory conditions are largely unknown. We previously identified transcription factor RBP-J as a key negative regulator that restrains TNF-\u03b1\u2013induced osteoclastogenesis and inflammatory bone resorption. In this study, we tested whether RBP-J suppresses inflammatory osteoclastogenesis by regulating the expression of microRNAs (miRNAs) important for this process. Using high-throughput sequencing of miRNAs, we obtained the first, to our knowledge, genome-wide profile of miRNA expression induced by TNF-\u03b1 in mouse bone marrow\u2013derived macrophages\/osteoclast precursors during inflammatory osteoclastogenesis. Furthermore, we identified miR-182 as a novel miRNA that promotes inflammatory osteoclastogenesis driven by TNF-\u03b1 and whose expression is suppressed by RBP-J. Downregulation of miR-182 dramatically suppressed the enhanced osteoclastogenesis program induced by TNF-\u03b1 in RBP-J\u2013deficient cells. Complementary loss- and gain-of-function approaches showed that miR-182 is a positive regulator of osteoclastogenic transcription factors NFATc1 and B lymphocyte\u2013induced maturation protein-1. Moreover, we identified that direct miR-182 targets, Foxo3 and Maml1, play important inhibitory roles in TNF-\u03b1\u2013mediated osteoclastogenesis. Thus, RBP-J\u2013regulated miR-182 promotes TNF-\u03b1\u2013induced osteoclastogenesis via inhibition of Foxo3 and Maml1. Suppression of miR-182 by RBP-J serves as an important mechanism that restrains TNF-\u03b1\u2013induced osteoclastogenesis. Our results provide a novel miRNA-mediated mechanism by which RBP-J inhibits osteoclastogenesis and suggest that targeting of the newly described RBP-J\u2013miR-182\u2013Foxo3\/Maml1 axis may represent an effective therapeutic approach to suppress inflammatory osteoclastogenesis and bone resorption.<\/jats:p>","DOI":"10.4049\/jimmunol.1502044","type":"journal-article","created":{"date-parts":[[2016,5,9]],"date-time":"2016-05-09T22:54:28Z","timestamp":1462834468000},"page":"4977-4986","source":"Crossref","is-referenced-by-count":64,"title":["RBP-J\u2013Regulated miR-182 Promotes TNF-\u03b1\u2013Induced Osteoclastogenesis"],"prefix":"10.1093","volume":"196","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2176-9516","authenticated-orcid":false,"given":"Christine H","family":"Miller","sequence":"first","affiliation":[{"name":"Arthritis and Tissue Degeneration Program, David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3460-3590","authenticated-orcid":false,"given":"Sinead M","family":"Smith","sequence":"additional","affiliation":[{"name":"Arthritis and Tissue Degeneration Program, David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahmoud","family":"Elguindy","sequence":"additional","affiliation":[{"name":"Arthritis and Tissue Degeneration Program, David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5396-918X","authenticated-orcid":false,"given":"Tuo","family":"Zhang","sequence":"additional","affiliation":[{"name":"Genomics Resources Core Facility, Weill Cornell Medical College , New York, NY 10065"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jenny Z","family":"Xiang","sequence":"additional","affiliation":[{"name":"Genomics Resources Core Facility, Weill Cornell Medical College , New York, NY 10065"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4289-6998","authenticated-orcid":false,"given":"Xiaoyu","family":"Hu","sequence":"additional","affiliation":[{"name":"Institute for Immunology and School of Medicine, Tsinghua University , Beijing 100084 ,","place":["China"]},{"name":"Collaborative Innovation Center for Biotherapy, Tsinghua University , Beijing 100084 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lionel B","family":"Ivashkiv","sequence":"additional","affiliation":[{"name":"Arthritis and Tissue Degeneration Program, David Z. 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