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- W2589059174 abstract "Purpose: Bone tissue engineering remains hampered by inadequate scaffold design and regulatory limitations on autologous cell use. We developed a novel system to silence and reactivate TGF-ß activating kinase 1 (TAK1), which mediates TGF-β1 and BMP2. We hypothesize that Tak1 can be initially silenced to increase local cell proliferation followed by Tak1 reactivation to stimulate bone differentiation, providing scaffold and cell-free bone healing. Methods: We developed a novel dual-recombinase system (Cre/lox; FLP/FRT) to allow silencing and reactivation of Tak1. Critical sized-calvarial defects were performed and mice received: 1. Ad.LacZ (control) 2. Ad.Cre (knockout) or 3. Ten days Ad.Cre (knockout) followed by Ad.FLP (reactivation) to modulate Tak1 expression. Cellular proliferation and differentiation were quantified histologically. MicroCT was used to quantify bone healing. In vitro studies with calvarial osteoblasts confirmed these findings. Results: Loss of Tak1 with Ad.Cre increased cellular proliferation (Ki67 immunostaining; Fig. 1A) while suppressing osteogenesis (Osterix immunostaining) within the defect. Ad.Cre followed by Ad.FLP stimulated increased cell proliferation followed by enhanced osteogenic differentiation. Timed Tak1 suppression followed by Tak1 activation improved bone healing compared to controls by microCT quantification. In vitro results (Fig. 1B, 1C) with calvarial osteoblasts were consistent with in vivo findings. Conclusion: These results validate that TAK1 can be mediated therapeutically to first potentiate cellular proliferation and then stimulate osteogenic differentiation to maximize bone healing without introducing exogenous scaffolds or cells." @default.
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- W2589059174 date "2017-02-01" @default.
- W2589059174 modified "2023-10-14" @default.
- W2589059174 title "Abstract 46. Modulating TAK1 Signaling to Enhance Scaffold and Cell-Free Calvarial Healing" @default.
- W2589059174 doi "https://doi.org/10.1097/01.gox.0000513461.84739.4e" @default.
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