The regenerative potential of tissue injury declines with age. Recently, a significant role for Wnt/β-catenin signaling has been shown in tissue specific stem cell aging, leading to increased tissue fibrosis. Wnt/β-catenin signaling regulates the differentiation of multipotent mesenchymal stem cells into osteoblasts during fracture repair. We investigated the potential role of dysregulated Wnt/β-catenin signaling in delayed fracture union and tissue fibrosis in the elderly. Old mice displayed increased total β-catenin protein levels at 4 and 7 days post-fracture and tissue fibrosis at 14 and 21 days post-fracture compared to young mice. Furthermore, treatment with a pharmalogical agent decreased total β-catenin protein levels in the fracture callus at 4 days post-fracture and prevented tissue fibrosis at 21 days post-fracture. Our data suggests that dysregulated Wnt/β-catenin signaling in the elderly contributes to delayed fracture repair and tissue fibrosis and offers a potential therapeutic strategy to improve fracture outcome in the elderly.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/25802 |
| Date | 11 January 2011 |
| Creators | Silkstone, David |
| Contributors | Benjamin, Alman |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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