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Reduction of the Wnt Inhibitor Dkk1 Correlates With Improved Bone Mechanical and Morphological Properties in Mice

[+] Author Affiliations
Danese M. Joiner, Steven A. Goldstein

University of Michigan, Ann Arbor, MI

Bryan T. MacDonald, Xi He, Peter V. Hauschka

Harvard Medical School, Boston, MA

Paper No. SBC2007-175478, pp. 859-860; 2 pages
doi:10.1115/SBC2007-175478
From:
  • ASME 2007 Summer Bioengineering Conference
  • ASME 2007 Summer Bioengineering Conference
  • Keystone, Colorado, USA, June 20–24, 2007
  • Conference Sponsors: Bioengineering Division
  • ISBN: 0-7918-4798-5
  • Copyright © 2007 by ASME

abstract

The Wnt/β-Catenin signaling pathway is a key regulator in bone development and bone homeostasis. Inactivating mutations in the Wnt co-receptor Low density lipoprotein Receptor related Protein 5 (LRP5) results in osteoporosis while “activating” mutations in LRP5 results in high bone mass. Dickkopf-1 (Dkk1) is a secreted Wnt inhibitor that binds to LRP5 and LRP6 reducing their availability to form a complex with Wnt and Frizzled and resulting in unrestrained Wnt signaling. It is expected that a decrease in Dkk1 will result in an increase in Wnt activity and ultimately a high bone mass phenotype. An allelic series of Dkk1 mutant mice were generated to examine the affects of reduced Dkk1 levels on bone density, morphology, and mechanical properties.

Copyright © 2007 by ASME
Topics: Bone

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