In Vivo Analysis of Wnt Signaling in Bone

Department of Genetics and Development, Columbia University, New York, New York, United States
Endocrinology (Impact Factor: 4.5). 06/2007; 148(6):2630-4. DOI: 10.1210/en.2006-1372
Source: PubMed


Bone remodeling requires osteoblasts and osteoclasts working in concert to maintain a constant bone mass. The dysregulation of signaling pathways that affect osteoblast or osteoclast differentiation or function leads to either osteopenia or high bone mass. The discovery that activating and inactivating mutations in low-density lipoprotein receptor-related protein 5, a putative Wnt coreceptor, led to high bone mass and low bone mass in human beings, respectively, generated a tremendous amount of interest in the possible role of the Wnt signaling pathway in the regulation of bone remodeling. A number of mouse models have been generated to study a collection of Wnt signaling molecules that have been identified as regulators of bone mass. These mouse models help establish the canonical Wnt signaling pathway as a major regulator of chondrogenesis, osteoblastogenesis, and osteoclastogenesis. This review will summarize these advances.

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    PLoS ONE 07/2014; 9(7):e98973. DOI:10.1371/journal.pone.0098973 · 3.23 Impact Factor
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    • "RANKL has been shown to activate mature osteoclasts and mediate osteoclastogenesis. OPG acts as a decoy receptor for RANKL [21]. The co-culture of PMOs and PC3 Hem cells produced an increase in RANKL and a decrease in OPG transcript levels in osteoblasts; the same result was observed after co-culture of PMOs with PC3 control cells (Figure 3 A&B). "
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    PLoS ONE 11/2013; 8(11):e80315. DOI:10.1371/journal.pone.0080315 · 3.23 Impact Factor
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    • "This protein activates canonical Wnt/β-catenin pathway [Ling et al., 2010], and its expression has been shown to occur related to osteoblast differentiation [Bain et al., 2003; Cho et al., 2009]. Wnt proteins signal by interacting with a cell membrane receptor complex comprising the Fzd family of receptors and co-receptors LRP-5 and LRP-6 [Glass and Karsenty, 2007; Mao et al., 2001a; Mao et al., 2001b]. A clear relationship exists between these co-receptors and the maintenance of bone mass as revealed by gain-or loss-of-function mutations affecting LRP-5 and LRP-6 genes in both mice and humans [Bodine and Komm, 2006]. "
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    Journal of Cellular Biochemistry 08/2013; 114(8). DOI:10.1002/jcb.24535 · 3.26 Impact Factor
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