| Autor: |
Bai, Xiao, Xi, Jie, Bi, Yanwen, Zhao, Xin, Bing, Weidong, Meng, Xiangbin, Liu, Yimin, Zhu, Zhonglai, Song, Guangmin |
| Předmět: |
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| Zdroj: |
Journal of Cellular & Molecular Medicine; Sep2017, Vol. 21 Issue 9, p2077-2091, 15p |
| Abstrakt: |
The oxidative stress caused by endothelial injury is involved in intimal hyperplasia ( IH) in vein grafts. Mesenchymal stem cells ( MSCs) can home to injured intima and promote endothelial repair. However, MSC apoptosis is increased accompanied by decreased functional activity under oxidative stress. Thus, we investigate whether tumour necrosis factor-α ( TNF-α) can promote the survival and activity of MSCs under oxidative stress to reduce IH more effectively, and establish what role the NF-κB pathway plays in this. In this study, we preconditioned MSCs with TNF-α ( TNF-α-PCMSCs) for 24 hrs and measured the activation of the IKK/ NF-κB pathway. EdU and transwell assays were performed to assess proliferation and migration of TNF-α-PCMSCs. Apoptosis and migration of TNF-α- PCMSCs were evaluated in conditions of oxidative stress by analysis of the expression of Bcl-2 and CXCR4 proteins. TNF-α- PCMSCs were transplanted into a vein graft model, so that cell homing could be tracked, and endothelial apoptosis and IH of vein grafts were measured. The results demonstrated that TNF-α promotes proliferation and migration of MSCs. Furthermore, survival and migration of TNF-α- PCMSCs under oxidative stress were both enhanced. A greater number of MSCs migrated to the intima of vein grafts after preconditioning with TNF-α, and the formation of neointima was significantly reduced. These effects could be partially abolished by IKK XII ( NF-κB inhibitor). All these results indicate that preconditioning with TNF-α can promote survival and migration of MSCs under oxidative stress via the NF-κB pathway and thus attenuate IH of vein grafts. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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