Apoptosis and arterial thrombosis: expression of CD31 and CD146 in recent and old thrombotic disorders

ABSTRACT

Apoptosis [programmed cell death] of vascular lining endothelium is one of the causes of increased thrombogenicity. The Luminal release of apoptotic endothelium-derived microparticles can cause activation of tissue factor [TF], the most potent known inhibitor of the blood clotting system. The study was carried out at Al-Azhar University Hospitals on 70 cases of arterial thrombosis above the age of 25 years Group 1 consisted of 15 apparently healthy subjects as a control group. Group 11 including 32 patients of recent thrombosis; 13 with cerebral infarction, 12 with acute myocardial in farction [MI] and 7 patients with peripheral arterial thrombosis. Group 111 including 38 patients with old thrombosis; 12 with cerebral infarction, 18 with MI and 8 patients with old peripheral arterial thrombosis. Endothelial-derived CD31 and CD146 were statistically higher in patients with recent and old arterial thrombosis than controls [p<0.005, p< 0.01] respectively and statistically higher in old than in recent arterial thrombosis [p<0.05]. Hypertension DM, smoking and lipid profile have no significant effect on CD31 and CD146. Finally, endothelial microparticle detection among cases of arterial thrombosis may indicate the persistence of the danger of re-thrombosis. Patients with acute and chronic ischemia have altered response of endothelial cells. It remains to be determined whether the reduction of the increased activity of CD31 and CD146 could provide an effective rationale for acute arterial thrombosis therapy