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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences Advance Access originally published online on July 8, 2009
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 2009 64A(10):1015-1024; doi:10.1093/gerona/glp089
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© The Author 2009. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Accelerated Features of Age-Related Bone Loss in Zmpste24 Metalloproteinase-Deficient Mice

Daniel Rivas1, Wei Li2,3, Rahima Akter1, Janet E. Henderson2 and Gustavo Duque1,3

1 Lady Davis Institute
2 JTN Wong Laboratories, McGill University, Montréal, Quebec, Canada
3 Aging Bone Research Program, Nepean Clinical School, University of Sydney, Penrith, New South Wales, Australia

Address correspondence to Gustavo Duque, MD, PhD, Aging Bone Research Program, Nepean Clinical School, University of Sydney, Level 5, South Block, Nepean Hospital, Penrith, NSW 2750, Australia. Email: gduque{at}med.usyd.edu.au


  Abstract

Age-related bone loss is associated with changes in bone cellularity, which include marrow fat infiltration and decreasing levels of osteoblastogenesis. The mechanisms that explain these changes remain unclear. Although nuclear lamina alterations occur in premature aging syndromes that include changes in body fat and severe osteoporosis, the role of proteins of the nuclear lamina in age-related bone loss remains unknown. Using the Zmpste24-null progeroid mice (Zmpste24–/–), which exhibit nuclear lamina defects and accumulate unprocessed prelamin A, we identified several alterations in bone cellularity in vivo. We found that defective prelamin A processing induced accelerated features of age-related bone loss including lower osteoblast and osteocyte numbers and higher levels of marrow adipogenesis. In summary, processing of prelamin A could become a new approach to regulate osteoblastogenesis and bone turnover and thus for the prevention and treatment of senile osteoporosis.

Keywords Lamin A/C; Osteoporosis; Mesenchymal stem cells; Osteoblastogenesis; Adipogenesis

Received: September 9, 2008; Accepted: February 15, 2009

Decision Editor: Huber R. Warner, PhD


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