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Updated: Jul 13, 2026

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
Published on: February 15, 2022
[Hyperplasia suppressor gene induces vascular smooth muscle cell apoptosis]
Yan Hong Guo1, Qian Li, Hai Yi Yu
1Department of Cardiology, Peking University Third Hospital, Beijing 100083, China.
Objective:
To study the effect of hyperplasia suppressor gene (HSG) in inducing vascular smooth muscle cell apoptosis and the underlying mechanisms.
Methods:
The cultured VSMCs were transfected with an adenoviral vector containing rat HSG gene. Effects of HSG on VSMC apoptosis were investigated by fluorescent dye staining to detect the tact of nuclei, and by flow cytometry to define the content of DNA and to detect the levels of caspase-3. The expressions of Bcl-2 and Bax were also performed by Western blot analysis.
Results:
The increased expression of HSG in VSMCs infected with AdHSG induced apoptotic cell death detected by flow cytometry assay and nucleic staining. Compared with control groups, HSG induced vascular smooth muscle cell apoptosis 72 h after infected with adenoviral vector (39.6%+/-3.2% vs. 2.6%+/-0.9%, P< 0.01). Overexpression of HSG also increased the activity of caspase-3 (0.354+/-0.104 vs. 0.064+/-0.022,P<0.01)and the release of cytochrome c. The Bcl-2 protein level was decreased ( 0.26+/-0.03 vs. 1.06+/-0.07,P<0.01)in AdHSG infected cells.
Conclusion:
Hyperplasia induced vascular smooth muscle cell apoptosis. HSG downregulated the expression of Bcl-2/Bax and activated caspase-3, and therefore promoted the release of cytochrome c and induced cell apoptosis.
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