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Abstract
To rescue the oxidative stress induced inhibition of osteogenesis, vitamin C (VC) was chemically modified onto three-dimensional graphene foams (3D GFs), then their regulation on osteogenesis of human bone marrow-derived mesenchymal stem cells (BM-MSCs) was studied. Combined action of VC + GF significantly decreased H2O2-induced oxidative stress, and rescued H2O2-inhibited cell viability, differentiation and osteogenesis of BM-MSCs in vitro. Further studies revealed that Wnt pathway may be involved in this protection of osteogenesis. Furthermore, an in vivo mouse model of BM-MSCs transplantation showed that VC + GF remarkably rescued oxidative stress inhibited calcium content and bone formation. The combination of VC and GF exhibited more pronounced protective effects against oxidative stress induced inhibition of osteogenesis, compared to monotherapy of VC or GF. Our study proposed a new strategy in stem cell-based therapies for treating bone diseases.
Highlights
The homeostasis of human bones is tightly balanced by the orchestrated activities of bone-forming osteoblasts and bone-resorbing osteoclasts
We investigated the osteogenesis of human bone marrow-derived mesenchymal stem cells (BM-Mesenchymal stem cells (MSCs)) in the culture directly. 0.2 mM H2O2 decreased the alkaline phosphatase (ALP) activity to approximately 42% after 8 days of differentiation (Figure 6A)
Numerous reports demonstrated that adverse oxidative stress inhibited osteogenesis of MSCs
Summary
The homeostasis of human bones is tightly balanced by the orchestrated activities of bone-forming osteoblasts and bone-resorbing osteoclasts. Oxidative stress, resulted from excessive reactive oxygen species (ROS) production, disrupts the homeostasis by inhibiting osteoblast function and stimulating osteoclastogenesis [1]. Oxidative stress was reported to be a major contributing factor of osteoporosis during aging [3, 4]. ROS, including superoxide anion, hydroxyl radical, hydroxyl ion, nitric oxide (NO) and hydrogen peroxide, react with DNA, protein and lipids inside cells, which further induces cytokine-mediated pro-inflammation. Excessive ROS are able to react with NO forming peroxynitrite that in turn could oxidize tetrahydrobiopterin, a cofactor of endothelial nitric oxide synthase (eNOS), and result in its decoupling from eNOS, leading to further elevated ROS, as well as decreased NO productions
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