J Korean Surg Soc.  2011 Apr;80(4):289-296. 10.4174/jkss.2011.80.4.289.

Association with inflammatory cells and apolipoproteins to the progression of atherosclerosis

• Eo HS
• Lee KB
• Kim AK
• Kim MH
• Kim DH
• Kim DI

• KMID: 1820021
• DOI: http://doi.org/10.4174/jkss.2011.80.4.289

Abstract

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 beta-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.

Keyword

Atherosclerosis; Inflammatory cells; Apolipoproteins; Senescence

MeSH Terms

Aging
Antibodies
Apolipoproteins
Apolipoproteins E
Atherosclerosis
Blotting, Western
Macrophages
Muscle, Smooth, Vascular
Plaque, Atherosclerotic
Rupture
Shoulder
T-Lymphocytes
Antibodies
Apolipoproteins
Apolipoproteins E

Figure

• 

  Fig. 1 Expressions of cluster of differentiation 68 (CD68), human telomerase reverse transcriptase (hTERT), apolipoprotein C1 (APO C1), and APO E in various lesions of atherosclerotic and non-atherosclerotic arteries. (A) Western blot analysis for the CD68, hTERT, APO C1, and APO E in non-atherosclerotic iliac arteries (lanes 1, 2), non-atherosclerotic carotid arteries (lanes 3, 4), the main lesion of the atheromas (lanes 5, 6), and the area adjacent to the atheromas (lane 7). Western blot results were the same for experiment five. (B) Specimens of carotid endarterectomy: ⓐ the main lesion of carotid atheroma and ⓑ the area adjacent to the atheroma.

• 

  Fig. 2 β-galactosidase (β-gal) activity in various arterial specimens (A) and β-gal and inmmunohistochemical staining in atherosclerotic plaques (B). (A) Photographs of the various arteries stained for β-gal activity (non-atherosclerotic iliac artery (1); endarterectomized carotid atheroma (2)). (B) The serial sections of the luminal layer of endarterectomized carotid atheroma stained for β-gal activity and immunohistochemistry stains for α-smooth muscle actin (3), CD3 (4), and CD68 (5). The (3), (4), and (5) were doble stained with β-gal and each antibody. The results were the same for experiment five (Magnification: ×40 for (3), (4), and (5); ×200 for (3-1), (4-1), and (5-1)).

• 

  Fig. 3 Immunohistochemistry for α-smooth muscle actin of vascular smooth muscle cells, cluster of differentiation 68 (CD68) of macrophages, CD3 of T-lymphocytes, apolipoprotein C1 (APO C1), and APO E in nonatherosclerotic arteries, 'focal' atherosclerotic plaques, and 'diffuse' atherosclerotic plaques in endarterectomized carotid atheroma. Arrows indicate the shoulder lesion of the atheromas. The results were the same for experiment five (Magnification, ×12.5). VSMC, vascular smooth muscle cell.

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