Abstract
BackgroundThe low survival rate or dysfunction of extracellular matrix (ECM)-based engineered organs caused by the adverse effects of unfavourable local microenvironments on seed cell viability and stemness, especially the effects of excessive reactive oxygen species (ROS), prompted us to examine the importance of controlling oxidative damage for tissue transplantation and regeneration. We sought to improve the tolerance of seed cells to the transplant microenvironment via antioxidant pathways, thus promoting transplant efficiency and achieving better tissue regeneration.MethodsWe improved the antioxidative properties of ECM-based bioroots with higher glutathione contents in dental follicle stem cells (DFCs) by pretreating cells or loading scaffolds with the antioxidant NAC. Additionally, we developed an in situ rat alveolar fossa implantation model to evaluate the long-term therapeutic effects of NAC in bioroot transplantation.ResultsThe results showed that NAC decreased H2O2-induced cellular damage and maintained the differentiation potential of DFCs. The transplantation experiments further verified that NAC protected the biological properties of DFCs by repressing replacement resorption or ankylosis, thus facilitating bioroot regeneration.ConclusionsThe following findings suggest that NAC could significantly protect stem cell viability and stemness during oxidative stress and exert better and prolonged effects in bioroot intragrafts.
Highlights
The low survival rate or dysfunction of extracellular matrix (ECM)-based engineered organs caused by the adverse effects of unfavourable local microenvironments on seed cell viability and stemness, especially the effects of excessive reactive oxygen species (ROS), prompted us to examine the importance of controlling oxidative damage for tissue transplantation and regeneration
To determine the appropriate drug concentrations, we performed a CCK-8 assay to measure the viability of hDFCs after they were incubated with different concentrations of H2O2 and NAC
Considering that cell death could interfere with the ROS and GSH measurements [28], 100 μmol/L H2O2 was used as the sublethal dose for the following experiments designed to establish the oxidative stress model
Summary
The low survival rate or dysfunction of extracellular matrix (ECM)-based engineered organs caused by the adverse effects of unfavourable local microenvironments on seed cell viability and stemness, especially the effects of excessive reactive oxygen species (ROS), prompted us to examine the importance of controlling oxidative damage for tissue transplantation and regeneration. Tissue necrosis caused by both oxidative stress and the inflammatory response further prevents nutrients and oxygen from reaching viable cells, which contributes to expanding the necrotic area and leads to implant failure [7]. The unfavourable microenvironment after isolation and transplantation reduces the stemness and inhibits the therapeutic effects of surviving seed cells in intragrafts [11]. Specific control of the balance within this cellular microenvironment may represent an efficient and novel strategy to increase the success rate of transplantation
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