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

Lei Jiao1, Ming Jiang1, Jun Liu1

  • 1Affiliated Hospital of Jiangsu University, Zhenjiang, PR China.

Vascular
|July 14, 2018
PubMed
Abstract

Insights

Nuclear factor-kappa B (NF-κB) activation inhibits vascular smooth muscle cell (VSMC) proliferation and promotes apoptosis. This effect is mediated by increased expression of FasL and the hypertension-related gene HRG-1.

Area of Science:

  • Vascular biology
  • Cell signaling
  • Molecular mechanisms

Background:

  • Vascular smooth muscle cells (VSMCs) play a critical role in cardiovascular health.
  • Dysregulation of VSMC proliferation and apoptosis contributes to vascular diseases.
  • The role of nuclear factor-kappa B (NF-κB) in VSMC behavior requires further elucidation.

Purpose of the Study:

  • To investigate the function of NF-κB in VSMC proliferation and apoptosis.
  • To explore the underlying molecular mechanisms of NF-κB action in VSMCs.
  • To assess the impact of NF-κB modulation on VSMC behavior.

Main Methods:

  • Human aorta VSMCs were utilized and divided into experimental groups including control, NF-κB inhibitor, and NF-κB overexpression.
  • Cell proliferation was assessed using the MTT assay.
  • Apoptosis was quantified by flow cytometry, and protein expression of NF-κB, FasL, and HRG-1 was determined via Western blotting.

Main Results:

  • NF-κB overexpression was successfully achieved and confirmed.
  • Activation of NF-κB significantly inhibited VSMC proliferation.
  • NF-κB overexpression markedly promoted VSMC apoptosis and upregulated the expression of FasL and HRG-1.

Conclusions:

  • Overexpression of NF-κB inhibits VSMC proliferation and induces apoptosis.
  • The pro-apoptotic and anti-proliferative effects of NF-κB in VSMCs are potentially mediated by the upregulation of FasL and HRG-1.
  • NF-κB represents a potential therapeutic target for vascular diseases characterized by VSMC dysfunction.

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