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CD 109 deficiency induces osteopenia with an osteoporosis‐like phenotype in vivo
Author(s) -
Mii Shinji,
Hoshino Akiyoshi,
Enomoto Atsushi,
Murakumo Yoshiki,
Ito Masako,
Yamaguchi Akira,
Takahashi Masahide
Publication year - 2018
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/gtc.12593
Subject(s) - bone remodeling , osteoclast , osteoporosis , osteopenia , bone resorption , endocrinology , medicine , biology , n terminal telopeptide , population , alkaline phosphatase , osteocalcin , bone mineral , biochemistry , receptor , environmental health , enzyme
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. CD 109 is a glycosylphosphatidylinositol‐anchored glycoprotein, a deficiency that leads to a psoriasis‐like skin inflammation in mice. Although the expression of CD 109 has been reported in mouse pre‐osteoclast cells, its function in osteoclasts in vivo remains largely unknown. To investigate the physiological role of CD 109 in bone metabolism, we analyzed bones from wild‐type and CD 109‐deficient adult mice. Micro‐computed tomography analysis of the femur (thigh bone) showed that bone volume was lower in CD 109‐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 CD 109‐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 CD 109‐deficient mice. These results indicate that CD 109 deficiency induces a high‐turnover, osteoporosis‐like phenotype, which suggests that CD 109 plays a role in bone metabolism in vivo.