Upregulation of endothelial adhesion molecules in hearts with congestive and ischemic cardiomyopathy: immunohistochemical evaluation of inflammatory endothelial cell activation

被引:23
作者
Wilhelmi, MH
Leyh, RG
Wilhelmi, M
Haverich, A
机构
[1] Leibniz Univ Hannover, Sch Med, Div Thorac & Cardiovasc Surg, D-30625 Hannover, Germany
[2] LEBAO, Hannover, Germany
关键词
cardiomyopathy; congestive heart disease; ischernic heart disease; immunology; adhesion molecules; endothelial cells;
D O I
10.1016/j.ejcts.2004.09.027
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: In recent years many data emphasized, that inflammatory reactions seem to be involved in the pathogenesis of ischemic (ICM) and congestive (CCM) heart disease. Since, it is well known that endothelial adhesion molecules play a pivotal rote in the initiation and maintenance of inflammatory reactions we therefore, evaluated the endothetial expression of a wide variety of different adhesion molecules in hearts suffering from ICM and CCM. Methods: Tissue samples from coronary arteries, and left and right ventricle myocardium originating form heart with ICM and CCM were evaluated. Tissue samples from healthy human donor hearts, which were not transplanted, served as controls. Evaluated adhesion molecule expression: selectin-family ELAM-1, CD62, immunoglobulin-supergene-family PECAM-1, ICAM-1, VCAM-1, integrin-family VLA-1,-2,-3,-4,-5, and -6, complementary-adhesion-molecules CD34, CD44 and the von-Willebrand-factor (vWF). Results: While endocardial surfaces and coronary arteries revealed only little differences when comparing tissue samples originating from healthy donor hearts and those suffering from ICM and CCM, significant differences were found within the myocardial microvasculature. Both kinds of diseased hearts showed stronger expressions for CD62, ELAM-1, ICAM-1 and VCAM-1 (only CCM) than controls. More and above, integrin molecules showed differential expressions too. Whereas, VLA-1 showed stronger expressions in diseased hearts, VLA-3,-5, and -6 were expressed much weaker in those hearts. Complementary adhesion molecules (CD34/CD44) did not show significant differences and the vWF was not found in any sample. Conclusions: Inflammatory reactions play a pivotal rote in the propagation and maintenance of both these cardiac detoriating diseases. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:122 / 127
页数:6
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