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Updated: Apr 27, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
[The phenotypic switching of vascular smooth muscle cells induced by cholesterol]
Bo Shu1, Yijun Yang2, Minzhang Qian2
1Shanghai University of Traditional Chinese Medicine, Shanghai 200032; Department of Biochemistry, Zunyi Medical College, Zunyi 563003, China.
Objective:
To observe the effect of cholesterol on phenotypic switching of human vascular smooth muscle cells (VSMCs) in vitro.
Methods:
VSMCs were treated with cholesterol at 12.5, 25.0 and 50.0 mg/L for 48 hours and at 50 mg/L for 24, 48 and 72 hours. Real-time quantitative PCR and Western blotting were respectively applied to detect the mRNA expressions of smooth muscle alpha-actin (α-SMA), smooth muscle 22 alpha (SM22α) and the protein expressions of SM22α, monocyte chemotactic protein-1 induced protein (MCPIP). CCK-8 assay was performed to analyze the viability of VSMCs.
Results:
Compared with control groups, cholesterol treatments resulted in a significant down-regulation of both mRNA and protein expressions of endogenous α-SMA and SM22α in VSMCs at 48 hours (P<0.05), and the expressions were lowest when cholesterol was 50.0 mg/L. At 48 and 72 hours, 50.0 mg/L cholesterol significantly decreased the expressions of α-SMA and SM22α (P<0.05). The proliferation of VSMCs in cholesterol groups was promoted significantly compared with control groups (P<0.05). Cholesterol at 50.0 mg/L was also able to induce MCPIP protein expression in VSMCs at 48 hours (P<0.05).
Conclusion:
Cholesterol can decrease the expressions of α-SMA and SM22α and enhance the proliferation of VSMCs, which suggests that cholesterol induces phenotypic switching of VSMCs.
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