Nuclear factor-kappa B activation inhibits proliferation and promotes apoptosis of vascular smooth muscle cells

  • Vascular. 2018 Dec;26(6):634-640. doi: 10.1177/1708538118787125.
Lei Jiao  1 Ming Jiang  1 Jun Liu  1 Lichao Wei  1 Min Wu  1
Affiliations
  • 1. Affiliated Hospital of Jiangsu University, Zhenjiang, PR China.
Abstract

Objectives: To investigate the role of nuclear factor-kappa B (NF-κB) performed in cell proliferation and Apoptosis of vascular smooth muscle cells (VSMCs), and to assess the mechanisms.

Methods: Human aorta VSMCs were divided into control, NF-κB Inhibitor, NF-κB overexpression + NF-κB Inhibitor, control vector + NF-κB Inhibitor, NF-κB overexpression, and control vector groups. NF-κB overexpression vector was constructed and transfected into VSMCs. Proliferation of VSMCs in each group was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide. Apoptosis of VSMCs was detected by flow cytometry. The expression of NF-κB, FasL, and hypertension-related gene (HRG-1) was measured by Western blotting.

Results: NF-κB overexpression vector was constructed correctly by Restriction Endonuclease, and the results showed that the activation of NF-κB could inhibit the proliferation of VSMCs. The results of flow cytometry also confirmed that NF-κB overexpression promoted Apoptosis of VSMCs. Mechanically, NF-κB overexpression could up-regulate the expression of FasL and HRG-1.

Conclusions: NF-κB overexpression promotes Apoptosis and inhibits cell proliferation of VSMCs. The mechanisms might be regulated by promoting FasL and HRG-1 expression.

Keywords
FasL; NF-κB; apoptosis; proliferation; vascular smooth muscle cells.
Products
  • Cat. No.
    Product Name
    Description
    Target
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  • 99.26%, IKKβ Inhibitor
    target: IKK
    Research Areas: Cancer