| First Author | Li X | Year | 2012 |
| Journal | Genes Cells | Volume | 17 |
| Issue | 7 | Pages | 568-75 |
| PubMed ID | 22646472 | Mgi Jnum | J:213981 |
| Mgi Id | MGI:5586963 | Doi | 10.1111/j.1365-2443.2012.01608.x |
| Citation | Li X, et al. (2012) Role of intercellular adhesion molecule-2 in osteoclastogenesis. Genes Cells 17(7):568-75 |
| abstractText | Osteoclasts, multinucleated bone-resorbing 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-1 (CD11b/CD18) during osteoclastogenesis. However, the counter receptor of Mac-1 was still unknown. Flow cytometric analysis showed that bone marrow-derived mononuclear cells, used as osteoclast precursors, expressed intercellular adhesion molecule-1 and -2. Quantitative RT-PCR analysis revealed that expression level of ICAM-2 was higher than that of ICAM-1 in bone marrow cells. The osteoclastogenesis induced by receptor activator of NF-kappaB ligand (RANKL) was inhibited by anti-ICAM-2 neutralizing antibody but not by anti-ICAM-1 neutralizing antibody. The inhibitory effect of anti-ICAM-2 antibody on osteoclastogenesis was enhanced by simultaneous treatment of anti-CD11b neutralizing antibody. Furthermore, osteoclastogenesis induced by tumor necrosis factor alpha (TNFalpha) was also inhibited by anti-ICAM-2 neutralizing antibody. The involvement of lymphocytes in osteoclastogenesis was excluded, because anti-ICAM-2 antibody inhibited osteoclastogenesis using bone marrow-derived cells from immunodeficiency mice. Immunocytochemical staining demonstrated colocalization of ICAM-2 and Mac-1 during osteoclastogenesis; however, Mac-1 immunoreactivity was lost in differentiated multinucleated osteoclast. These results suggest the important role of ICAM-2/Mac-1 binding in osteoclastogenesis induced by either RANKL or TNFalpha. |
