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

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 b...

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Autores principales: Brum, Andrea M, van der Leije, Cindy S, Schreuders‐Koedam, Marijke, Chaibi, Siham, van Leeuwen, Johannes PTM, van der Eerden, Bram CJ
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6237209/
https://www.ncbi.nlm.nih.gov/pubmed/30460337
http://dx.doi.org/10.1002/jbm4.10061
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author Brum, Andrea M
van der Leije, Cindy S
Schreuders‐Koedam, Marijke
Chaibi, Siham
van Leeuwen, Johannes PTM
van der Eerden, Bram CJ
author_facet Brum, Andrea M
van der Leije, Cindy S
Schreuders‐Koedam, Marijke
Chaibi, Siham
van Leeuwen, Johannes PTM
van der Eerden, Bram CJ
author_sort Brum, Andrea M
collection PubMed
description 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. © 2018 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
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spelling pubmed-62372092018-11-20 Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging Brum, Andrea M van der Leije, Cindy S Schreuders‐Koedam, Marijke Chaibi, Siham van Leeuwen, Johannes PTM van der Eerden, Bram CJ JBMR Plus Original Articles 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. © 2018 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research. John Wiley and Sons Inc. 2018-07-14 /pmc/articles/PMC6237209/ /pubmed/30460337 http://dx.doi.org/10.1002/jbm4.10061 Text en © 2018 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Brum, Andrea M
van der Leije, Cindy S
Schreuders‐Koedam, Marijke
Chaibi, Siham
van Leeuwen, Johannes PTM
van der Eerden, Bram CJ
Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging
title Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging
title_full Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging
title_fullStr Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging
title_full_unstemmed Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging
title_short Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging
title_sort mucin 1 (muc1) deficiency in female mice leads to temporal skeletal changes during aging
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6237209/
https://www.ncbi.nlm.nih.gov/pubmed/30460337
http://dx.doi.org/10.1002/jbm4.10061
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