Relationship of Angiopoietin-2 Expression to Atherosclerosis in Middle Cerebral and Coronary Arteries.
- Author:
Eun Kyung SHIN
1
;
Jae Wook PARK
;
Min Chul PARK
;
Chan Woong KIM
;
Jun Suk AHN
;
Kyeong Han PARK
;
Dae Joong KIM
;
Jang Hee HAHN
;
Gou Young KOH
;
Jeong Hyun PARK
Author Information
1. Department of Anatomy, College of Medicine, Kangwon National University, Korea. jhpark@kangwon.ac.kr
- Publication Type:Original Article
- Keywords:
Middle cerebral artery;
Coronary artery;
Ang-2;
Atherosclerosis
- MeSH:
Angiogenesis Inducing Agents;
Angiopoietin-2*;
Arteries;
Atherosclerosis*;
Cerebral Arteries;
Classification;
Constriction, Pathologic;
Coronary Artery Disease;
Coronary Vessels*;
Endothelial Cells;
Endothelium;
Humans;
Incidence;
Intracranial Arteriosclerosis;
Macrophages;
Middle Cerebral Artery;
Paraffin;
Phenobarbital;
Plaque, Atherosclerotic
- From:Korean Journal of Anatomy
2006;39(4):269-278
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Atherosclerosis is a systemic and multifactorial disease, its incidence is raised recently. Cerebral and coronary atherosclerosis have some similar pathogenesis, but their relationship and mechanisms are still remain unclear. Intimal neovascularization in the atherosclerotic plaque was focused with respect to its pathological roles, intimal thickening and atherosclerotic progression. Ang-2, which is an angiogenesis regulating factor, provides a destabilizing signal for endothelial cells, leading to vessel regression or sprouting. However the role and distribution of Ang-2 in atherosclerotic coronary and cerebral arteries are still not well known. Thus, we analyzed 1) atherosclerotic lesion progression 2) relationship of atherosclerosis to Ang-2 expression in human middle cerebral and coronary artery. Paraffin sections from 25 human coronary (COA) and 36 middle cerebral arteries (MCA) were characterized according to AHA classification. In the same person, the score of atherosclerosis progression in COA was higher than that of MCA. In the two kinds of arteries having same atherosclerotic progression, the degree of intimal proliferation and luminal stenosis in COA was higher than that of MCA. Expression of Ang-2 was not shown in normal artery but localized in lumen-lining endothelium, macrophage in preatheroma, atheroma and complicated lesion. Ang-2 expression and infiltration of macrophages were rich in COA than MCA. Our result indicated that cerebral atherosclerosis has some different pathogenic mechanisms with coronary atherosclerosis according to difference of progression and angiogenic factor Ang-2 expression. Thus this is a fundamental study for understanding the progression of atherosclerosis in different vascular beds.
