{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,9]],"date-time":"2025-11-09T07:41:12Z","timestamp":1762674072944,"version":"build-2065373602"},"reference-count":56,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2016,4,27]],"date-time":"2016-04-27T00:00:00Z","timestamp":1461715200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>CD97, a member of the 7\u2010transmembrane epidermal growth factor family of adhesion G protein\u2013coupled receptors, is expressed on various cell types. This study was undertaken to elucidate the functions of CD97 in bone and inflammation in an experimental mouse model, by examining the effect of CD97 on osteoclastogenesis in vitro, characterizing the skeletal phenotype of CD97\u2010deficient (CD97\u2010knockout [KO]) mice, and assessing the responses to tumor necrosis factor (TNF) treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Femoral tissue and bone marrow (BM)\u2013derived cells from CD97\u2010KO and wild\u2010type (WT) mice were assessed using histomorphometric analyses, in vitro cultures, and reverse transcription\u2013polymerase chain reaction. Serum cytokine and chemokine levels in the presence or absence of TNF challenge were analyzed by multiplex assay.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In cultures of mouse BM\u2010derived macrophages in vitro, RANKL induced the expression of CD97. In vivo, the trabecular bone volume of the femurs of female CD97\u2010KO mice was increased, and this was associated with a decrease in the number of osteoclasts. Compared to WT mice, CD97\u2010KO mice had a reduced potential to form osteoclast\u2010like cells in vitro. Furthermore, TNF treatment augmented the formation of osteoclasts in the calvaria of CD97\u2010KO mice in vivo, by increasing the production of RANKL and other cytokines and chemokines and by reducing the production of osteoprotegerin by calvarial cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings demonstrate that CD97 is a positive regulator of osteoclast\u2010like cell differentiation, a mechanism that influences bone homeostasis. However, the presence of CD97 may be essential to suppress the initial osteoclastogenesis that occurs in response to acute and local inflammatory stimuli.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.39538","type":"journal-article","created":{"date-parts":[[2015,12,14]],"date-time":"2015-12-14T10:55:43Z","timestamp":1450090543000},"page":"1301-1313","source":"Crossref","is-referenced-by-count":14,"title":["Contradictory Role of CD97 in Basal and Tumor Necrosis Factor\u2013Induced Osteoclastogenesis In Vivo"],"prefix":"10.1002","volume":"68","author":[{"given":"Hee Yeon","family":"Won","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Se Hwan","family":"Mun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bongjin","family":"Shin","sequence":"additional","affiliation":[{"name":"University of Connecticut Health Center 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