Open Access

Nrf2 protects against diabetic dysfunction of endothelial progenitor cells via regulating cell senescence

  • Authors:
    • Rui‑Yun Wang
    • Li‑Hua Liu
    • Hongxia Liu
    • Ke‑Fei Wu
    • Jing An
    • Qian Wang
    • Yun Liu
    • Li‑Juan Bai
    • Ben‑Ming Qi
    • Ben‑Ling Qi
    • Lei Zhang
  • View Affiliations

  • Published online on: June 11, 2018     https://doi.org/10.3892/ijmm.2018.3727
  • Pages: 1327-1340
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Diabetes is associated with an increased risk of cardiovascular disease. A decrease in the number and functionality of endothelial progenitor cells (EPCs) leads to reduced endothelial repair and the development of cardiovascular disease. The aim of the present study was to explore the effect and underlying mechanisms of nuclear factor erythroid 2‑related factor 2 (Nrf2) on EPC dysfunction caused by diabetic mellitus. The biological functions of EPCs in streptozotocin‑induced diabetic mice were evaluated, including migration, proliferation, angiogenesis and the secretion of vascular endothelial growth factor (VEGF), stromal‑derived growth factor (SDF) and nitric oxide (NO). Oxidative stress levels in diabetic EPCs were also assessed by detecting intracellular reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA). EPC senescence was evaluated by measuring p16 and b‑gal expression and observing the senescence‑associated secretory phenotype. In addition, the function of EPCs and level of oxidative stress were assessed following Nrf2 silencing or activation. Nrf2 silencing resulted in a decrease of EPC biological functions, accelerated cell senescence and increased oxidative stress, as indicated by ROS and MDA upregulation accompanied with decreased SOD activity. Furthermore, Nrf2 silencing inhibited migration, proliferation and secretion in EPCs, while it increased oxidative stress and cell senescence. Nrf2 activation protected diabetic EPCs against the effects of oxidative stress and cell senescence, ameliorating the biological dysfunction of EPCs derived from mice with diabetes. In conclusion, Nrf2 overexpression protected against oxidative stress‑induced functional damage in EPCs derived from diabetic mice by regulating cell senescence.
View Figures
View References

Related Articles

Journal Cover

September-2018
Volume 42 Issue 3

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

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Wang RY, Liu LH, Liu H, Wu KF, An J, Wang Q, Liu Y, Bai LJ, Qi BM, Qi BL, Qi BL, et al: Nrf2 protects against diabetic dysfunction of endothelial progenitor cells via regulating cell senescence. Int J Mol Med 42: 1327-1340, 2018
APA
Wang, R., Liu, L., Liu, H., Wu, K., An, J., Wang, Q. ... Zhang, L. (2018). Nrf2 protects against diabetic dysfunction of endothelial progenitor cells via regulating cell senescence. International Journal of Molecular Medicine, 42, 1327-1340. https://doi.org/10.3892/ijmm.2018.3727
MLA
Wang, R., Liu, L., Liu, H., Wu, K., An, J., Wang, Q., Liu, Y., Bai, L., Qi, B., Qi, B., Zhang, L."Nrf2 protects against diabetic dysfunction of endothelial progenitor cells via regulating cell senescence". International Journal of Molecular Medicine 42.3 (2018): 1327-1340.
Chicago
Wang, R., Liu, L., Liu, H., Wu, K., An, J., Wang, Q., Liu, Y., Bai, L., Qi, B., Qi, B., Zhang, L."Nrf2 protects against diabetic dysfunction of endothelial progenitor cells via regulating cell senescence". International Journal of Molecular Medicine 42, no. 3 (2018): 1327-1340. https://doi.org/10.3892/ijmm.2018.3727