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Int. J. Mol. Sci. 2013, 14(11), 22149-22162; doi:10.3390/ijms141122149
Article

The Protective Effect of Bcl-xl Overexpression against Oxidative Stress-Induced Vascular Endothelial Cell Injury and the Role of the Akt/eNOS Pathway

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Received: 21 September 2013; in revised form: 26 October 2013 / Accepted: 30 October 2013 / Published: 8 November 2013
(This article belongs to the Section Molecular Pathology)
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Abstract: Restenosis after intraluminal or open vascular reconstruction remains an important clinical problem. Vascular endothelial cell (EC) injury induced by oxidative stress plays an important role in the development of intimal hyperplasia. In this study, we sought to evaluate the protective effects of Bcl-xl overexpression in vitro on oxidative stress-induced EC injury and the role of the Akt/endothelial nitric oxide synthase (eNOS) pathway. Human umbilical vein endothelial cells (HUVECs) exposed to hydrogen peroxide (H2O2, 0.5 mM) were used as the experimental oxidative stress model. The Bcl-xl gene was transferred into HUVECs through recombinant adenovirus vector pAdxsi-GFP-Bcl-xl before oxidative treatment. Cell apoptosis was evaluated by Annexin V/propidium iodide and Hoechst staining, caspase-7 and PARP cleavage. Cell viability was assessed using the cell counting kit-8 assay, proliferating cell nuclear antigen (PCNA) immunocytochemical detection and the scratching assay. Expressions of Akt, phospho-Akt and eNOS were detected by Western blotting. Our results showed that H2O2 induced apoptosis and decreased the cell viability of HUVECs. Bcl-xl overexpression significantly protected cells from H2O2-induced cell damage and apoptosis and maintained the cell function. Furthermore, the level of phospho-Akt and eNOS protein expression was significantly elevated when pretreated with Bcl-xl gene transferring. These findings suggest that Bcl-xl overexpression exerts an anti-apoptotic and protective effect on EC function. The Akt/eNOS signaling pathway is probably involved in these processes.
Keywords: vascular endothelial cells; oxidative stress; intimal hyperplasia; gene therapy; apoptosis vascular endothelial cells; oxidative stress; intimal hyperplasia; gene therapy; apoptosis
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Ni, L.; Li, T.; Liu, B.; Song, X.; Yang, G.; Wang, L.; Miao, S.; Liu, C. The Protective Effect of Bcl-xl Overexpression against Oxidative Stress-Induced Vascular Endothelial Cell Injury and the Role of the Akt/eNOS Pathway. Int. J. Mol. Sci. 2013, 14, 22149-22162.

AMA Style

Ni L, Li T, Liu B, Song X, Yang G, Wang L, Miao S, Liu C. The Protective Effect of Bcl-xl Overexpression against Oxidative Stress-Induced Vascular Endothelial Cell Injury and the Role of the Akt/eNOS Pathway. International Journal of Molecular Sciences. 2013; 14(11):22149-22162.

Chicago/Turabian Style

Ni, Leng; Li, Tianjia; Liu, Bao; Song, Xitao; Yang, Genhuan; Wang, Linfang; Miao, Shiying; Liu, Changwei. 2013. "The Protective Effect of Bcl-xl Overexpression against Oxidative Stress-Induced Vascular Endothelial Cell Injury and the Role of the Akt/eNOS Pathway." Int. J. Mol. Sci. 14, no. 11: 22149-22162.


Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert