{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T19:16:50Z","timestamp":1791919010983,"version":"4.3.4"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,1,15]],"date-time":"2022-01-15T00:00:00Z","timestamp":1642204800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100005150","name":"Chinese Academy of Medical Sciences","doi-asserted-by":"publisher","award":["2019PT320003"],"award-info":[{"award-number":["2019PT320003"]}],"id":[{"id":"10.13039\/501100005150","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81960401"],"award-info":[{"award-number":["81960401"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2022,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Bone loss is a hallmark of inflammatory bone diseases caused by aberrantly activated osteoclasts (OCLs). Studies have shown that OCLs exhibit various phenotypes and functions due to variations in the source(s) of precursor cells, cytokine expressions, and microenvironment\u2010dependent factors. During these conditions, inflammatory osteoclasts (iOCLs) lose their immune\u2010suppressive effect relative to OCLs under physiological conditions. This induces TNF \u03b1\u2010producing CD4\n                    <jats:sup>+<\/jats:sup>\n                    T\u00a0cells in an antigen\u2010dependent manner and finally leads to cascade amplification of iOCLs. OCL\u2010derived exosomes have been reported to regulate OCL formation and inhibit the osteoblast activity. However, the specific function and mechanism of iOCL\u2010derived exosomes on osteoblast have not been studied yet. In the present study, we compare the osteoblast promoting activities of iOCL\u2010derived exosomes and OCL\u2010derived exosomes. We found that iOCLs exosomes specifically target osteoblasts through ephrinA2\/EphA2. Mechanistically, the lncRNA LIOCE is enriched in iOCL exosomes and promotes the osteoblast activity after being incorporated into osteoblasts. Furthermore, our results revealed that exosomal lncRNA LIOCE stabilizes osteogenic transcription factor Osterix by interacting and reducing the ubiquitination level of Osterix. This study demonstrated that the bone loss is alleviated in the inflammatory osteolysis mice model after injection of iOCL exosomes encapsulating lncRNA LIOCE. The role of exosomes encapsulating lncRNA LIOCE in promoting bone formation was well established in the rat bone repair model. Our results indicate that iOCL\u2010derived exosomal lncRNA LIOCE promotes bone formation by upregulating Osx expression, and thus, the exosomes encapsulating lncRNA LIOCE may be an effective strategy to increase bone formation in osteoporosis and other bone metabolic disorders.\n                  <\/jats:p>","DOI":"10.1096\/fj.202101106rr","type":"journal-article","created":{"date-parts":[[2022,1,15]],"date-time":"2022-01-15T11:59:11Z","timestamp":1642247951000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Inflammatory osteoclasts\u2010derived exosomes promote bone formation by selectively transferring lncRNA LIOCE into osteoblasts to interact with and stabilize Osterix"],"prefix":"10.1096","volume":"36","author":[{"given":"Lingyan","family":"Ren","sequence":"first","affiliation":[{"name":"Medical College Guizhou University  Guiyang China"},{"name":"Department of Orthopedics Guizhou Provincial People's 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