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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Association with inflammatory cells and apolipoproteins to the progression of atherosclerosis
Hyun-Seon Eo1, Kyung-Bok Lee, Ae-Kyeong Kim
1Division of Vascular Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Insights
Inflammatory cells like macrophages and T-cells, along with apolipoproteins C1 and E, are elevated in atherosclerosis. Their senescence contributes to plaque progression by expanding the necrotic core.
Area of Science:
- Cardiovascular Biology
- Immunology
- Atherosclerosis Research
Background:
- Inflammatory cells are implicated in atherosclerosis progression and plaque rupture.
- The specific roles of inflammatory cells and apolipoproteins in atherosclerosis development remain unclear.
Purpose of the Study:
- To investigate the differential expression of inflammatory cells in atherosclerosis.
- To evaluate the impact of apolipoprotein (APO) C1 and APO E on atherosclerosis progression.
Main Methods:
- Comparative analysis of 10 atherosclerotic and 5 non-atherosclerotic tissues.
- Identification of vascular smooth muscle cells (VSMCs), macrophages, T-cells, APO C1, and APO E using Western blotting and immunohistochemistry.
- Assessment of cellular senescence via senescence-associated β-galactosidase staining.
Main Results:
- Macrophages, APO C1, and APO E showed significantly higher expression and senescence in atherosclerotic lesions.
- Macrophage and T-cell infiltration increased from early to advanced atherosclerotic plaques.
- APO C1 localized to the necrotic core, while APO E was found around the core and fibrous cap in advanced plaques.
Conclusions:
- Macrophage and T-cell expression and senescence correlate with APO C1 and APO E induction and deposition.
- These factors contribute to atherosclerotic plaque development and progression, particularly by expanding the necrotic core.
Purpose:
Inflammatory cells are known to be associated with the progression of atherosclerosis and plaque rupture. However, the relation to inflammatory cells and apolipoproteins on the progression of atherosclerosis is unknown. This study was aimed at examining the different expressions of inflammatory cells and evaluate the effect of apolipoprotein (APO) C1 and APO E during the progression of atherosclerosis.
Methods:
Ten atherosclerotic tissues were compared with five non-atherosclerotic tissues. The presence of vascular smooth muscle cells (VSMCs), macrophages, T-cells, APO C1, and APO E were identified by Western blotting and immunohistochemical analysis with antibodies. The senescence was analyzed by senescence-associated β-galactosidase.
Results:
The protein expression and senescence of macrophages, APO C1 and APO E were significantly higher in the main atherosclerotic lesion than the non-atherosclerotic lesion. A high concentration of inflammatory cells and the paucity of VSMCs were present in the shoulder area. In addition, macrophage and T-cells are expressed in the early stage of atherosclerotic development and more expanded in advanced atherosclerotic plaques. APO C1 was expressed mainly within the necrotic core, and APO E existed mostly around the necrotic core and the fibrous cap in advanced atherosclerotic plaques.
Conclusion:
Our study indicated that the expression and the senescence of macrophage and T-cells may be closelyrelated to induction and deposition of APO C1 and APO E. This contributes to the development and progression of atherosclerotic plaque by expanding the necrotic core.
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