{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T20:20:49Z","timestamp":1789935649485,"version":"4.0.1"},"reference-count":25,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,5,31]],"date-time":"2012-05-31T00:00:00Z","timestamp":1338422400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes to Cells"],"published-print":{"date-parts":[[2012,7]]},"abstract":"<jats:p>Osteoclasts, multinucleated bone\u2010resorbing cells, are specialized cells derived from the monocyte\/macrophage lineage. Therefore, it is essential for mononuclear precursors to find a fusion partner during its differentiation. Our previous study showed an important role of cell communication via Mac\u20101 (<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>11b\/<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>18) during osteoclastogenesis. However, the counter receptor of Mac\u20101 was still unknown. Flow cytometric analysis showed that bone marrow\u2010derived mononuclear cells, used as osteoclast precursors, expressed intercellular adhesion molecule\u20101 and \u20102. Quantitative <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> analysis revealed that expression level of <jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20102 was higher than that of <jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20101 in bone marrow cells. The osteoclastogenesis induced by receptor activator of <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010kappaB ligand (<jats:styled-content style=\"fixed-case\">RANKL<\/jats:styled-content>) was inhibited by anti\u2010<jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20102 neutralizing antibody but not by anti\u2010<jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20101 neutralizing antibody. The inhibitory effect of anti\u2010<jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20102 antibody on osteoclastogenesis was enhanced by simultaneous treatment of anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>11b neutralizing antibody. Furthermore, osteoclastogenesis induced by tumor necrosis factor \u03b1 (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u03b1) was also inhibited by anti\u2010<jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20102 neutralizing antibody. The involvement of lymphocytes in osteoclastogenesis was excluded, because anti\u2010<jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20102 antibody inhibited osteoclastogenesis using bone marrow\u2010derived cells from immunodeficiency mice. Immunocytochemical staining demonstrated colocalization of <jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20102 and Mac\u20101 during osteoclastogenesis; however, Mac\u20101 immunoreactivity was lost in differentiated multinucleated osteoclast. These results suggest the important role of <jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20102\/Mac\u20101 binding in osteoclastogenesis induced by either <jats:styled-content style=\"fixed-case\">RANKL<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u03b1.<\/jats:p>","DOI":"10.1111\/j.1365-2443.2012.01608.x","type":"journal-article","created":{"date-parts":[[2012,5,31]],"date-time":"2012-05-31T09:05:54Z","timestamp":1338455154000},"page":"568-575","source":"Crossref","is-referenced-by-count":10,"title":["Role of intercellular adhesion molecule\u20102 in osteoclastogenesis"],"prefix":"10.1111","volume":"17","author":[{"given":"Xianglan","family":"Li","sequence":"first","affiliation":[{"name":"Department of Cellular Physiological Chemistry Graduate School Tokyo Medical and Dental University  1\u20105\u201045, Yushima Bunkyo\u2010ku Tokyo 113\u20108549 Japan"},{"name":"Department of Obstetrics and Gynecology Juntendo University School of Medicine  2\u20101\u20101, Hongo Bunkyo\u2010ku Tokyo 113\u20108421 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masako","family":"Akiyama","sequence":"additional","affiliation":[{"name":"Department of Cellular Physiological Chemistry Graduate School Tokyo Medical and Dental University  1\u20105\u201045, Yushima Bunkyo\u2010ku Tokyo 113\u20108549 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ken\u2010ichi","family":"Nakahama","sequence":"additional","affiliation":[{"name":"Department of Cellular Physiological Chemistry Graduate School Tokyo Medical and Dental University  1\u20105\u201045, Yushima Bunkyo\u2010ku Tokyo 113\u20108549 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taro","family":"Koshiishi","sequence":"additional","affiliation":[{"name":"Department of Cellular Physiological Chemistry Graduate School Tokyo Medical and Dental University  1\u20105\u201045, Yushima Bunkyo\u2010ku Tokyo 113\u20108549 Japan"},{"name":"Department of Obstetrics and Gynecology Juntendo University School of Medicine  2\u20101\u20101, Hongo Bunkyo\u2010ku Tokyo 113\u20108421 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoru","family":"Takeda","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology Juntendo University School of Medicine  2\u20101\u20101, Hongo Bunkyo\u2010ku Tokyo 113\u20108421 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ikuo","family":"Morita","sequence":"additional","affiliation":[{"name":"Department of Cellular Physiological Chemistry Graduate School Tokyo Medical and Dental University  1\u20105\u201045, Yushima Bunkyo\u2010ku Tokyo 113\u20108549 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