Journal Article

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

Daniel Rivas, Wei Li, Rahima Akter, Janet E. Henderson and Gustavo Duque

in The Journals of Gerontology: Series A

Volume 64A, issue 10, pages 1015-1024
Published in print October 2009 | ISSN: 1079-5006
Published online July 2009 | e-ISSN: 1758-535X | DOI: http://dx.doi.org/10.1093/gerona/glp089
Accelerated Features of Age-Related Bone Loss in Zmpste24 Metalloproteinase-Deficient Mice

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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

Journal Article.  5705 words.  Illustrated.

Subjects: Geriatric Medicine ; Public Health ; Biological Sciences ; Molecular and Cell Biology ; Neuroscience

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