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Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification.


ABSTRACT: Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG-/- mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.

SUBMITTER: Bucay N 

PROVIDER: S-EPMC316769 | biostudies-literature | 1998 May

REPOSITORIES: biostudies-literature

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osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification.

Bucay N N   Sarosi I I   Dunstan C R CR   Morony S S   Tarpley J J   Capparelli C C   Scully S S   Tan H L HL   Xu W W   Lacey D L DL   Boyle W J WJ   Simonet W S WS  

Genes & development 19980501 9


Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG-/- mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-  ...[more]

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