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Benzo[a]pyrene induces oxidative stress and endothelial progenitor cell dysfunction via the activation of the NF-κB pathway

  • Authors:
    • Kangting Ji
    • Cheng Xing
    • Fengchun Jiang
    • Xiaoyan Wang
    • Huihui Guo
    • Jinliang Nan
    • Lu Qian
    • Penglin Yang
    • Jiafeng Lin
    • Meide Li
    • Jinnong Li
    • Lianming Liao
    • Jifei Tang

  • View Affiliations

  • Published online on: February 26, 2013     https://doi.org/10.3892/ijmm.2013.1288
  • Pages: 922-930
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Abstract

Smoking is a major risk factor for atherosclerosis. In this study, we evaluated the effects of benzo[a]pyrene (BaP, a prominent component of tobacco smoke) on the function and pro-inflammatory response of human endothelial progenitor cells (EPCs). EPCs were isolated from umbilical cord blood and treated with different concentrations (10, 20 and 50 µmol/l) of BaP. The proliferation, migration, adhesion and angiogenesis of BaP-treated EPCs were evaluated using the cell counting kit-8 (CCK-8), Transwell assay, adhesion assay and in vitro tube formation assay, respectively. The activation of nuclear factor-κB (NF-κB) was evaluated by measuring the mRNA expression of NF-κB p65 and p50 by real-time RT-PCR and NF-κB translocation assay. Reactive oxygen species (ROS) production was determined by the reduction of fluorescent 2',7'-dichlorofluorescein diacetate (DCFH-DA). The results demonstrated that BaP treatment significantly inhibited the proliferation, migration, adhesion and angiogenesis of EPCs in vitro. In addition, BaP induced the release of interleukin (IL)-1β and tumor necrosis factor-α from these cells. Moreover, the exposure of EPCs to BaP induced ROS generation and the activation of NF-κB. Experiments with EPCs pre-treated with pyrrolidine dithiocarbamate, an inhibitor of NF-κB, revealed that the BaP-mediated inhibition of proliferation, migration, adhesion and angiogenesis of EPCs is mainly regulated by NF-κB. Thus, tobacco smoke may induce oxidant-mediated stress responses in EPCs and impair their function via the activation of the NF-κB pathway.
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April 2013
Volume 31 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

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  • Journal Metrics
  • Impact Factor: 5.7
  • Ranked Medicine Research and Experimental
    (total number of cites)
  • CiteScore: 12.3
  • CiteScore Rank: Q1: #28/347 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 1.022
  • SCImago Journal Rank (SJR): 1.167
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Spandidos Publications style
Ji K, Xing C, Jiang F, Wang X, Guo H, Nan J, Qian L, Yang P, Lin J, Li M, Li M, et al: Benzo[a]pyrene induces oxidative stress and endothelial progenitor cell dysfunction via the activation of the NF-κB pathway. Int J Mol Med 31: 922-930, 2013.
APA
Ji, K., Xing, C., Jiang, F., Wang, X., Guo, H., Nan, J. ... Tang, J. (2013). Benzo[a]pyrene induces oxidative stress and endothelial progenitor cell dysfunction via the activation of the NF-κB pathway. International Journal of Molecular Medicine, 31, 922-930. https://doi.org/10.3892/ijmm.2013.1288
MLA
Ji, K., Xing, C., Jiang, F., Wang, X., Guo, H., Nan, J., Qian, L., Yang, P., Lin, J., Li, M., Li, J., Liao, L., Tang, J."Benzo[a]pyrene induces oxidative stress and endothelial progenitor cell dysfunction via the activation of the NF-κB pathway". International Journal of Molecular Medicine 31.4 (2013): 922-930.
Chicago
Ji, K., Xing, C., Jiang, F., Wang, X., Guo, H., Nan, J., Qian, L., Yang, P., Lin, J., Li, M., Li, J., Liao, L., Tang, J."Benzo[a]pyrene induces oxidative stress and endothelial progenitor cell dysfunction via the activation of the NF-κB pathway". International Journal of Molecular Medicine 31, no. 4 (2013): 922-930. https://doi.org/10.3892/ijmm.2013.1288