Related Experiment Video
Updated: Jun 15, 2025
A Method to Study the Correlation Between Local Collagen Structure and Mechanical Properties of Atherosclerotic Plaque Fibrous Tissue
Published on: November 11, 2022
Syndecan-1 as a predictor of vulnerable atherosclerotic plaques
Yan Qiu1,2, Zhi Ouyang1, Jian Zhong1
1Institute of Biomedical Engineering, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, China.
Insights
Syndecan-1 (SDC-1) is elevated in atherosclerosis, correlating with plaque vulnerability. This study identifies SDC1 as a potential biomarker for cardiovascular disease, aiding in risk assessment and treatment strategies.
Area of Science:
- Cardiovascular Biology
- Atherosclerosis Research
- Proteoglycan Function
Background:
- Atherosclerosis (AS) is a major cause of cardiovascular disease, with vulnerable plaques driving acute events.
- Syndecan-1 (SDC-1), a vascular endothelial glycocalyx proteoglycan, is implicated in plaque progression, but its role in plaque vulnerability is unclear.
Purpose of the Study:
- To investigate Syndecan-1 (SDC-1) expression in atherosclerosis.
- To determine the correlation between SDC-1 and atherosclerotic plaque vulnerability in a mouse model.
Main Methods:
- ApoE-/- mice were subjected to high-fat diet and/or carotid artery ligation to induce AS.
- Immunohistochemistry and immunofluorescence analyzed plaque composition, SDC-1 expression, and vulnerability markers.
- Serum levels of SDC1, sphingosine 1-phosphate (S1P), and VEGF-A were measured.
Main Results:
- AS induction led to increased plaque vulnerability, lipid accumulation, and macrophage infiltration.
- SDC-1 expression was significantly higher in AS plaques and positively correlated with plaque vulnerability.
- Elevated serum SDC1, S1P, and VEGF-A were observed in AS mice, correlating with plaque vulnerability.
- Multivariate analysis identified SDC1 as an independent predictor of plaque vulnerability.
Conclusions:
- SDC-1 is upregulated in vulnerable atherosclerotic plaques.
- Serum SDC1 shows potential as a clinical biomarker for assessing atherosclerosis severity and vulnerability.
- Targeting SDC1 or related pathways may offer new therapeutic strategies for cardiovascular disease.
Aims:
Cardiovascular disease remains a major global health concern, with atherosclerosis (AS) being a significant contributor. Vulnerable plaques play a critical role in acute cardiovascular events. Syndecan-1 (SDC-1), a vital membrane proteoglycan in the vascular endothelial glycocalyx, is believed to be associated with plaque progression. However, its precise relationship with severity and vulnerability of atherosclerotic plaque remains unclear. This study aimed to investigate SDC-1 expression and its potential correlation with plaque vulnerability in ApoE-/- atherosclerosis mouse model.
Methods And Results:
Eight-week-old mice were induced into the AS model using a high-fat diet (HFD) and/or partial ligation of the left common carotid artery (PLCA), with a chow diet (CD) control group. After 16 weeks, plaques in the aortic root showed the following order: HFD + PLCA group > HFD group > CD + PLCA group > CD group. Immunohistochemistry revealed heightened accumulation of lipid/foam cells and CD68-labeled macrophages in the plaques, elevated vascular endothelial growth factor (VEGF), and matrix Metalloproteinase-9 (MMP-9) in the HFD + PLCA group's plaques, along with reduced collagen and α-SMA-labeled smooth muscle cells, resulting in the highest vulnerability index value. Immunohistofluorescence analysis of frozen plaque sections showed significantly higher SDC-1 expression in the AS mice group compared to the CD group, both positively correlated with plaque vulnerability. Serum analysis demonstrated elevated levels of SDC1, sphingosine 1-phosphate (S1P), and VEGF-A in the AS mice, all positively correlated with plaque vulnerability. Multivariate analysis identified SDC1 as an independent predictor of plaque vulnerability.
Conclusion:
This study enhances our understanding of plaque vulnerability mechanisms and presents SDC1 as a potential biomarker for atherosclerosis. These findings underscore the importance of addressing modifiable risk factors, such as diet and hemodynamics and suggest the utility of serum SDC1 as a valuable clinical marker. Ultimately, these insights may lead to more effective strategies in combating cardiovascular diseases and improving patient outcomes.
