| First Author | Mii S | Year | 2018 |
| Journal | Genes Cells | Volume | 23 |
| Issue | 7 | Pages | 590-598 |
| PubMed ID | 29767469 | Mgi Jnum | J:272760 |
| Mgi Id | MGI:6282344 | Doi | 10.1111/gtc.12593 |
| Citation | Mii S, et al. (2018) CD109 deficiency induces osteopenia with an osteoporosis-like phenotype in vivo. Genes Cells 23(7):590-598 |
| abstractText | Osteoporosis is a global public health problem that is increasing along with an aging population. A major determinant of osteoporosis is high bone turnover, which results from osteoclast activation. CD109 is a glycosylphosphatidylinositol-anchored glycoprotein, a deficiency that leads to a psoriasis-like skin inflammation in mice. Although the expression of CD109 has been reported in mouse pre-osteoclast cells, its function in osteoclasts in vivo remains largely unknown. To investigate the physiological role of CD109 in bone metabolism, we analyzed bones from wild-type and CD109-deficient adult mice. Micro-computed tomography analysis of the femur (thigh bone) showed that bone volume was lower in CD109-deficient mice than in wild-type mice. Bone histomorphometric analysis showed not only a reduction in bone volume but also an increase in bone turnover in CD109-deficient mice as compared with wild-type mice. Additionally, we measured serum levels of several markers of bone turnover and found a significant increase in the N-terminal telopeptide of type I collagen, a bone resorption marker, as well as alkaline phosphatase, a bone formation marker, in CD109-deficient mice. These results indicate that CD109 deficiency induces a high-turnover, osteoporosis-like phenotype, which suggests that CD109 plays a role in bone metabolism in vivo. |
