Osteoprotegerin and Soluble TRAIL Serum Levels in Patients with Coronary Artery Disease | ||||
Bulletin of Egyptian Society for Physiological Sciences | ||||
Article 11, Volume 26, Issue 2, December 2006, Page 159-176 PDF (179.98 K) | ||||
Document Type: Original Article | ||||
DOI: 10.21608/besps.2006.37536 | ||||
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Authors | ||||
Amal El-Shehaby* 1; Mona Nabih2; Nehad Tawfik2; Ahmed Abd el-Aziz3; Amr El-Hadiday3 | ||||
1Medical Biochemistry, Department, Faculty of Medicine - Cairo University | ||||
2Internal Medicine Department, Faculty of Medicine - Cairo University | ||||
3Critical Care Department, Faculty of Medicine - Cairo University | ||||
Abstract | ||||
Osteoprotegerin (OPG) is a key factor in bone remodelling (inhibitor of osteoclastogenesis), a member of the tumour necrosis factor receptor family, and also a decoy receptor for the receptor activator of nuclear factor kappa-B ligand (RANKL) and tumour necrosis factor- related apoptosis inducing ligand (TRAIL) was recently implicated in human atherogenesis. OPG could be produced by cells of the cardiovascular system, including coronary artery smooth muscle cells and endothelial cells and may operate in vascular physiopathology regulating vascular calcification, apoptosis and immune defense raising the possibility that alterations of OPG serum levels may be associated with coronary artery disease (CAD). The present work was intended to assess the possible role of serum OPG and s-TRAIL in the pathology of CAD. Since OPG acts by neutralizing TRAIL we hypothesized that serum levels of TRAIL are also altered in vascular disease. Eighty male subjects were included in this study categorized into three groups: 28 patients with acute myocardial infarction (AMI), 32 patients with established stable CAD and 20 healthy males serving as control subjects. All groups were matched for age and body mass index. Following clinical evaluation, blood samples were withdrawn for serum OPG & s-TRAIL determination using enzyme linked immunosorbent assay (ELISA). In the present study, both AMI and stable CAD groups exhibited significantly higher serum OPG levels compared to control subjects. On the other hand, both AMI and stable CAD groups showed significantly lower serum s-TRAIL levels compared to control subjects.Furthermore, in the AMI group there was a significantly higher serum OPG and lower s-TRAIL levels compared to stable CAD group. Also, it was found that there is a progressive increase in serum OPG levels and decrease in s-TRAIL levels as the number of affected coronary vessels increase in both AMI and stable CAD groups. In conclusion, the present data showed a close association between raised serum OPG and reduced s-TRAIL in patients with CAD (both AMI and stable CAD). In view of the pro-apoptotic effects of TRAIL on vascular smooth muscle and endothelial cells, an elevation of circulating OPG levels may represent a crucial compensatory mechanism to limit further vascular damage. | ||||
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