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Updated: Feb 7, 2026

Measuring Proliferation of Vascular Smooth Muscle Cells Using Click Chemistry
Published on: October 30, 2019
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.
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.
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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