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Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
Published on: February 15, 2022
The rhythmic expression of clock genes attenuated in human plaque-derived vascular smooth muscle cells
Changpo Lin, Xiao Tang, Zhu Zhu
1Institute of Vascular Surgery, Department of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China. rzqian@shmu.edu.cn.
Insights
Human plaque-derived vascular smooth muscle cells (VSMCs) exhibit altered circadian rhythms and clock gene expression compared to normal VSMCs. These changes may contribute to atherosclerosis and plaque rupture.
Area of Science:
- Cardiovascular Biology
- Chronobiology
- Molecular Medicine
Background:
- Cardiovascular events like myocardial infarction and stroke exhibit a morning peak, suggesting circadian rhythm involvement.
- Peripheral tissues and cells, including vascular smooth muscle cells (VSMCs), possess intrinsic clock systems.
- Investigating circadian rhythmicity in VSMCs is crucial for understanding cardiovascular disease pathogenesis.
Purpose of the Study:
- To determine if primary cultured human plaque-derived VSMCs exhibit circadian rhythmicity.
- To compare the expression of clock genes between normal and plaque-derived human carotid VSMCs.
- To elucidate the role of circadian clock gene dysregulation in atherosclerosis.
Main Methods:
- Primary human carotid VSMCs were cultured from atherosclerotic plaques and normal carotid arteries.
- Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was employed to measure mRNA levels of clock genes.
- Serum shock was used to synchronize cellular circadian rhythms.
Main Results:
- Both normal and plaque-derived VSMCs displayed circadian expression of Bmal1, Cry1, Cry2, Per1, Per2, Per3, and Rev-erbα mRNA after serum shock.
- Clock mRNA showed rhythmic expression in plaque-derived VSMCs but not in normal VSMCs.
- Expression levels of key clock genes were significantly lower in plaque-derived VSMCs, and the Bmal1 rhythm was altered.
Conclusions:
- Human plaque-derived VSMCs demonstrate distinct circadian rhythmicity compared to normal VSMCs.
- Altered circadian rhythmicity and clock gene expression in plaque-derived VSMCs may play a role in atherosclerosis development.
- These findings suggest that circadian dysregulation in VSMCs could promote plaque rupture.
Background:
Acute myocardial infarction and stroke are more likely to occur in the early morning. Circadian pacemakers are considered to be involved in the process. Many peripheral tissues and cells also contain clock systems. In this study, we examined whether the primary cultured human plaque-derived vascular smooth muscle cells (VSMCs) process circadian rhythmicity; furthermore, we investigated the expression difference of clock genes between normal human carotid VSMCs and human plaque-derived VSMCs.
Methods:
Fifty-six human carotid plaques provided the atherosclerotic tissue, and 21 samples yielded viable cultured primary VSMCs. The normal carotid VSMCs were cultured from donors' normal carotids. The mRNA levels of the target genes were measured by Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR).
Results:
After serum shock, both types of cells showed clear circadian expressions of Bmal1, Cry1, Cry2, Per1, Per2, Per3 and Rev-erbα mRNA; meanwhile the Clock mRNA show a rhythmic expression in plaque-derived SMCs but not in normal carotid VSMCs. The expression levels of these main clock genes were significantly attenuated in human plaque-derived VSMCs compared with normal human carotid VSMCs. The rhythm of Bmal1 mRNA in plaque-derived VSMCs was changed.
Conclusion:
The present results demonstrate that the human plaque-derived VSMCs possess different circadian rhythmicity from that of normal carotid VSMCs. The rhythm changes of clock genes in plaque-derived VSMCs may be involved in the process of atherosclerosis and finally promote the rupture of plaque.
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