Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging

Andrea M. Brum, Cindy S. Van der Leije, Marijke Schreuders-Koedam, Siham Chaibi, Johannes Ptm Van Leeuwen, Bram Cj Van der Eerden*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

5 Citations (Scopus)
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Abstract

Mucin1 (MUC1) encodes a glycoprotein that has been demonstrated to have important roles in cell-cell interactions, cell-matrix interactions, cell signaling, modulating tumor progression and metastasis, and providing physical protection to cells against pathogens. In this study, we investigated the bone phenotype in female C57BL/6 Muc1 null mice and the impact of the loss of Muc1 on osteoblasts and osteoclasts. We found that deletion of Muc1 results in reduced trabecular bone volume in 8-week-old mice compared with wild-type controls, but the trabecular bone volume fraction normalizes with increasing age. In mature female mice (16 weeks old), Muc1 deletion results in stiffer femoral bones with fewer osteoblasts lining the trabecular surface but increased endosteal mineralized surface and bone formation rate. The latter remains higher compared with wild-type females at age 52 weeks. No difference was found in osteoclast numbers in vivo and in bone marrow osteoblast or osteoclast differentiation capacity or activity in vitro. Taken together, these results suggest that Muc1 depletion causes a transiently reduced trabecular bone mass phenotype in young mice, and later in life reduced numbers of osteoblasts with increased endocortical mineralization activity coincides with unaffected total bone mass and increased stiffness. In conclusion, our results show, for the first time to our knowledge, a role for Muc1 in bone mass and mineralization in mice in a time-dependent manner. (C) 2018 The Authors JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
Original languageEnglish
Pages (from-to)341-350
Number of pages10
JournalJBMR Plus
Volume2
Issue number6
DOIs
Publication statusPublished - Nov 2018

Research programs

  • EMC MM-01-39-02

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