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Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells

  • Authors:
    • Wei Li
    • Da‑Yong Du
    • Yang Liu
    • Feng Jiang
    • Pan Zhang
    • Yun‑Tian Li
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, 305 Hospital of the People's Liberation Army, Beijing 100017, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 85-90
    |
    Published online on: November 18, 2016
       https://doi.org/10.3892/etm.2016.3916
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Abstract

Endothelial progenitor cells (EPCs) have an important role in maintaining endothelial homeostasis. Previous studies reported that smoking has detrimental effects on EPCs; however, recent studies revealed that short‑term nicotine exposure may benefit EPCs. As most smokers are exposed to nicotine over an extended time period, the present study aimed to investigate the long‑term effects of nicotine on EPCs. Mice were administered nicotine orally for 1, 3 or 6 months. The mice exposed to nicotine for 1 month demonstrated increased EPC counts and telomerase activity and reduced cell senescence compared with control mice, consistent with previous reports. However, long‑term nicotine exposure resulted in opposing effects on EPCs, causing decreased counts, functional impairment and reduced telomerase activity. Furthermore, the effects of nicotine exposure were correlated with changes in sirtuins type 1 (SIRT1) protein expression. The current study indicated that long‑term nicotine exposure induces dysfunction and senescence of EPCs, which may be associated with impairment of telomerase activity through SIRT1 downregulation. The present results emphasize the necessity of smoking cessation to prevent dysfunction of EPCs.
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Copy and paste a formatted citation
Spandidos Publications style
Li W, Du DY, Liu Y, Jiang F, Zhang P and Li YT: Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells. Exp Ther Med 13: 85-90, 2017.
APA
Li, W., Du, D., Liu, Y., Jiang, F., Zhang, P., & Li, Y. (2017). Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells. Experimental and Therapeutic Medicine, 13, 85-90. https://doi.org/10.3892/etm.2016.3916
MLA
Li, W., Du, D., Liu, Y., Jiang, F., Zhang, P., Li, Y."Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells". Experimental and Therapeutic Medicine 13.1 (2017): 85-90.
Chicago
Li, W., Du, D., Liu, Y., Jiang, F., Zhang, P., Li, Y."Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells". Experimental and Therapeutic Medicine 13, no. 1 (2017): 85-90. https://doi.org/10.3892/etm.2016.3916
Copy and paste a formatted citation
x
Spandidos Publications style
Li W, Du DY, Liu Y, Jiang F, Zhang P and Li YT: Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells. Exp Ther Med 13: 85-90, 2017.
APA
Li, W., Du, D., Liu, Y., Jiang, F., Zhang, P., & Li, Y. (2017). Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells. Experimental and Therapeutic Medicine, 13, 85-90. https://doi.org/10.3892/etm.2016.3916
MLA
Li, W., Du, D., Liu, Y., Jiang, F., Zhang, P., Li, Y."Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells". Experimental and Therapeutic Medicine 13.1 (2017): 85-90.
Chicago
Li, W., Du, D., Liu, Y., Jiang, F., Zhang, P., Li, Y."Long‑term nicotine exposure induces dysfunction of mouse endothelial progenitor cells". Experimental and Therapeutic Medicine 13, no. 1 (2017): 85-90. https://doi.org/10.3892/etm.2016.3916
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