CD109 deficiency induces osteopenia with an osteoporosis-like phenotype in vivo

Genes to Cells : Devoted to Molecular & Cellular Mechanisms
Shinji MiiMasahide Takahashi

Abstract

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...Continue Reading

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Citations

Aug 29, 2019·Annals of the Rheumatic Diseases·Guanhua SongJinxiang Han
Apr 3, 2021·Developmental Dynamics : an Official Publication of the American Association of Anatomists·John B Pawlak, Gerard C Blobe

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