| First Author | Mizuhashi K | Year | 2012 |
| Journal | Dev Growth Differ | Volume | 54 |
| Issue | 4 | Pages | 474-80 |
| PubMed ID | 22416756 | Mgi Jnum | J:204884 |
| Mgi Id | MGI:5543589 | Doi | 10.1111/j.1440-169X.2012.01333.x |
| Citation | Mizuhashi K, et al. (2012) OBIF, an osteoblast induction factor, plays an essential role in bone formation in association with osteoblastogenesis. Dev Growth Differ 54(4):474-80 |
| abstractText | In vertebrate bone formation, the functional mechanisms of transcription factors in osteoblastic differentiation have been relatively well elucidated; however, the exact roles of cell-extrinsic molecules are less clear. We previously identified human and mouse Obif, an osteoblast induction factor, also known as Tmem119, which encodes a single transmembrane protein. OBIF is predominantly expressed in osteoblasts in mouse. While exogenous Obif expression stimulated osteoblastic differentiation, knockdown of Obif inhibits the osteoblastic differentiation of pre-osteoblastic MC3T3-E1 cells. In order to investigate an in vivo role of OBIF in bone formation, we generated Obif-deficient mice by targeted gene disruption. Analyses of micro-computed tomography (mCT) revealed that Obif(-/-) mice exhibit significantly reduced cortical thickness in the mid-shaft of the femur at postnatal day 14 (P14). Furthermore, progressive bone hypoplasia is observed after 8 weeks. The expression levels of osteoblast marker genes, Collagen 1a1, Osteopontin, Runx2, and Osterix, in the calvaria were decreased in Obif(-/-) mice at P4. These data indicate that Obif plays an essential role in bone formation through regulating osteoblastogenesis. |
