Expression of endothelial cell adhesion molecules on heart valves: up-regulation in degeneration as well as acute endocarditis

Citation
Am. Muller et al., Expression of endothelial cell adhesion molecules on heart valves: up-regulation in degeneration as well as acute endocarditis, J PATHOLOGY, 191(1), 2000, pp. 54-60
Citations number
57
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF PATHOLOGY
ISSN journal
00223417 → ACNP
Volume
191
Issue
1
Year of publication
2000
Pages
54 - 60
Database
ISI
SICI code
0022-3417(200005)191:1<54:EOECAM>2.0.ZU;2-N
Abstract
Inflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis fac tor-alpha (TNF-alpha), as well as shear stress, cause endothelial cells (EC s), to undergo not only functional alterations but also structural reorgani zations, which contribute to vascular leakage, Like ECs of the human aorta, ECs on heart valves are exposed to extreme shear stress. However, while EC s expression of cell adhesion molecules (CAMs) in large vessels has been wi dely studied, it seems that there are no such studies on ECs of heart valve s, although this knowledge might be important for our understanding of the aetiological aspects of local inflammatory responses. Using immunohistochem istry, this study characterized the CAM expression of ECs on degenerative, mostly calcified heart valves and on heart valves with florid endocarditis. As expected, the constitutively expressed molecules (ICAM-1, CD34, CD31) w ere found both on degenerative and on inflamed valves. Furthermore, marked expression of E-selectin and VCAM-1 was found not only on inflamed valves, but also on larger portions of the degenerative valves with no morphologica l evidence of inflammation. This striking finding might help to explain why patients with fibrotic heart valves are susceptible to recurrent endocardi tis. Why the endothelial activation markers E-selectin and VCAM-1 are expre ssed on degenerative heart valves requires further investigation. Copyright (C) 2000 John Wiley & Sons, Ltd.