{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T06:30:38Z","timestamp":1790836238642,"version":"4.1.0"},"reference-count":33,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2020,9,13]],"date-time":"2020-09-13T00:00:00Z","timestamp":1599955200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biomedical Materials Res"],"published-print":{"date-parts":[[2021,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>After bone prosthesis replacement, M1\u2010type macrophage polarization can be induced by titanium (Ti) particles and produce inflammatory, leading to osteolysis. Adipocyte\u2010derived exosomes (ADEs) exert immune\u2010modulatory impact on the macrophage, while whether it can inhibit the macrophage polarization induced by Ti is unclear. This study focuses on the M1\u2010type macrophage and aims to determine the effect of ADEs on Ti\u2010induced M1\u2010type macrophage polarization in osteolytic mice and the involved mechanism.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Ti particle\u2010induced osteolysis mouse model was established and macrophages were isolated from the osteolysis site. The levels of NLRP3 and specific markers for M1\u2010type macrophage were determined. ADEs isolated from adipocyte cell line 3T3\u2010L1, or conditioned ADEs with low\u2010expressed miR\u201034a isolated from 3T3\u2010L1 transfected with miR\u201034a inhibitor were co\u2010cultured with RAW 264.7 to determine their impact on the polarization of macrophage.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>ADEs reduced the M1\u2010type macrophage polarization and caused the upregulation of miR\u201034a in macrophage of the osteolysis site of the osteolysis mouse model. Also, the level of miR\u201034a in ADEs was higher than that in the adipocyte. The conditioned ADEs expressed a low level of miR\u201034a and boosted the Ti\u2010induced M1\u2010type polarization. MiR\u201034a could target NLRP3 and negatively regulated its expression. Moreover, NLRP3 knockdown in macrophage restricted the conditioned ADEs to promote macrophage towards to Ti\u2010induced M1\u2010type polarization. The inhibitory function of ADEs on M1\u2010type macrophage polarization was abolished by miR\u201034a silencing in the mouse osteolysis model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The miR\u201034a carried by ADEs reduced the polarization of M1\u2010type macrophages by targeting macrophage NLRP3 during Ti particle\u2010induced osteolysis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jbm.a.37088","type":"journal-article","created":{"date-parts":[[2020,8,28]],"date-time":"2020-08-28T04:45:42Z","timestamp":1598589942000},"page":"994-1003","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["<scp>miR<\/scp>\u201034a carried by adipocyte exosomes inhibits the polarization of <scp>M1<\/scp> macrophages in mouse osteolysis 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