Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells

  • Authors:
    • Nao Yan
    • Wei Yang
    • Xiao Dong
    • Qiao Fang
    • Yi Gong
    • Jian‑Liang Zhou
    • Jian‑Jun Xu
  • View Affiliations

  • Published online on: August 31, 2017     https://doi.org/10.3892/etm.2017.5083
  • Pages: 4595-4601
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Previous studies have demonstrated that nicotinamide phosphoribosyltransferase (NAMPT) promoted inflammation and permeability of vascular endothelial cells following cardiopulmonary bypass (CPB). In addition, mitogen‑activated protein kinase (MAPK) signaling was activated and contributed to these cell responses. However, the mechanism by which NAMPT regulates cellular inflammation and permeability remains unknown, and whether NAMPT regulates MAPK signaling during this process is also not clear. The present study established an anoxia‑reoxygenation (A‑R) model using human umbilical vein endothelial cells (HUVECs) and investigated the regulation of MAPK signaling by NAMPT by using small RNA transfection, ELISA and western blot analysis. The results demonstrated that A‑R significantly induced the expression levels of NAMPT and cellular permeability‑associated proteins, and the release of several inflammatory factors. Furthermore, calcium and MAPK signaling were evidently increased. When the A‑R cells were transfected with NAMPT small interfering RNA, the expression of cellular permeability‑associated proteins was downregulated, the release of inflammatory factors was decreased, and calcium and MAPK signaling was blocked. These data suggest that NAMPT may activate MAPK signaling to promote A‑R‑induced inflammation and permeability enhancement of HUVECs. Therefore, the current study indicates that NAMPT may be a potential drug target for A‑R‑induced endothelial cell injury subsequent to CPB.
View Figures
View References

Related Articles

Journal Cover

November-2017
Volume 14 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Yan N, Yang W, Dong X, Fang Q, Gong Y, Zhou JL and Xu JJ: Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells. Exp Ther Med 14: 4595-4601, 2017
APA
Yan, N., Yang, W., Dong, X., Fang, Q., Gong, Y., Zhou, J., & Xu, J. (2017). Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells. Experimental and Therapeutic Medicine, 14, 4595-4601. https://doi.org/10.3892/etm.2017.5083
MLA
Yan, N., Yang, W., Dong, X., Fang, Q., Gong, Y., Zhou, J., Xu, J."Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells". Experimental and Therapeutic Medicine 14.5 (2017): 4595-4601.
Chicago
Yan, N., Yang, W., Dong, X., Fang, Q., Gong, Y., Zhou, J., Xu, J."Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells". Experimental and Therapeutic Medicine 14, no. 5 (2017): 4595-4601. https://doi.org/10.3892/etm.2017.5083