Vol 9: Preconditioning of Mesenchymal Stem Cells by Sevoflurane to Improve Their Therapeutic Potential.Report as inadecuate



 Vol 9: Preconditioning of Mesenchymal Stem Cells by Sevoflurane to Improve Their Therapeutic Potential.


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This article is from PLoS ONE, volume 9.AbstractBackground: Bone marrow mesenchymal stem cells MSCs have been found to produce beneficial effects on ischemia-reperfusion injury. However, most of the MSCs died when transplanted into the ischemic tissue, which severely limit their therapeutic potential. Methods: Using an in vitro model of hypoxia and serum deprivation H-SD, we investigated the hypothesis that sevoflurane preconditioning could protect MSCs against H-SD-induced apoptosis and improve their migration, proliferation, and therapeutic potential. The H-SD of MSCs and neuron-like PC12 cells were incubated in a serum-free medium and an oxygen concentration below 0.1% for 24 h. Sevoflurane preconditioning was performed through a 2-h incubation of MSCs in an airtight chamber filled with 2 vol% sevoflurane. Apoptosis of MSCs or neuron-like PC12 cells was assessed using Annexin V-FITC-propidium iodide PI. Furthermore, the mitochondrial membrane potential was assessed using lipophilic cationic probe. The proliferation rate was evaluated through cell cycle analysis. Finally, HIF-1α, HIF-2α, VEGF and p-Akt-Akt levels were measured by western blot. Results: Sevoflurane preconditioning minimized the MSCs apoptosis and loss of mitochondrial membrane potential. Furthermore, it increased the migration and expression of HIF-1α, HIF-2α, VEGF, and p-Akt-Akt, reduced by H-SD. In addition, neuron-like PC12 cells were more resistant to H-SD-induced apoptosis when they were co-cultured with sevoflurane preconditioning MSCs. Conclusion: These findings suggest that sevoflurane preconditioning produces protective effects on survival and migration of MSCs against H-SD, as well as improving the therapeutic potential of MSCs. These beneficial effects might be mediated at least in part by upregulating HIF-1α, HIF-2α, VEGF, and p-Akt-Akt.



Author: Sun, Xuejun; Fang, Bo; Zhao, Xi; Zhang, Guangwei; Ma, Hong

Source: https://archive.org/







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