BACKGROUND: Acute thrombosis after atherosclerotic plaques disruption is a major complication of primary atherosclerosis, leading to acute ischemic syndromes and atherosclerotic progression. Vitronectin (VN) is multifunctional glycoprotein in blood and in the extracellular matrix. It binds glycosaminoglycans, collagen, plasminogen and urokinase receptor. VN stabilizes the inhibitory confirmation of plasminogen activation inhibitor-1 (PAI-1). Vitronectin may control the clearance of vascular thrombi by binding and stabilizing PAI-1, a key regulator of fibrinolysis. Therefore, VN is generally regarded as a cofactor for PAI-1 activity. On the other hand vitronectin binds to platelet glycoproteins may mediate platelet adhesion and aggregation at sites of vascular injury. Previous studies showed that anti-VN antibodies inhibit platelet aggregation in vitro, suggesting that vitronectin contributes to platelet accumulation at sites of vascular injury. In this study; we investigated the levels of plasma vitronectin in patients with Coronary Artery Disease (CAD) and control group. METHODS: The patient group was divided into four subgroups: patients with no, single, double and triple vessel disease according to their angiography results. ELISA procedure (Technoclone) was used to determine the plasma vitronectin levels. RESULTS: Plasma vitronectin levels in patient with CAD (% 125.87 +/- 58.38) were found to be significantly higher than control group (% 89.47 +/- 25.3) (p:0.000). In addition, in patients with double vessel disease (% 146.03 +/- 71.69) plasma vitronectin levels were significantly higher than no vessel disease (% 87.84 +/- 22.30) and control group, triple vessel disease (% 160.81 +/- 57.02) significantly higher as compare with no, single vessel disease (% 111.68 +/- 45.34) and control group (p < 0.05). There was no correlation between vitronectin and lipid parameters. CONCLUSION: These findings suggested that vitronectin is a marker of CAD. Elevated levels may indicate its role in the genesis and/or progression of CAD or may be the results of a compensatory mechanism.
BACKGROUND: Acute thrombosis after atherosclerotic plaques disruption is a major complication of primary atherosclerosis, leading to acute ischemic syndromes and atherosclerotic progression. Vitronectin (VN) is multifunctional glycoprotein in blood and in the extracellular matrix. It binds glycosaminoglycans, collagen, plasminogen and urokinase receptor. VN stabilizes the inhibitory confirmation of plasminogen activation inhibitor-1 (PAI-1). Vitronectin may control the clearance of vascular thrombi by binding and stabilizing PAI-1, a key regulator of fibrinolysis. Therefore, VN is generally regarded as a cofactor for PAI-1 activity. On the other hand vitronectin binds to platelet glycoproteins may mediate platelet adhesion and aggregation at sites of vascular injury. Previous studies showed that anti-VN antibodies inhibit platelet aggregation in vitro, suggesting that vitronectin contributes to platelet accumulation at sites of vascular injury. In this study; we investigated the levels of plasma vitronectin in patients with Coronary Artery Disease (CAD) and control group. METHODS: The patient group was divided into four subgroups: patients with no, single, double and triple vessel disease according to their angiography results. ELISA procedure (Technoclone) was used to determine the plasma vitronectin levels. RESULTS: Plasma vitronectin levels in patient with CAD (% 125.87 +/- 58.38) were found to be significantly higher than control group (% 89.47 +/- 25.3) (p:0.000). In addition, in patients with double vessel disease (% 146.03 +/- 71.69) plasma vitronectin levels were significantly higher than no vessel disease (% 87.84 +/- 22.30) and control group, triple vessel disease (% 160.81 +/- 57.02) significantly higher as compare with no, single vessel disease (% 111.68 +/- 45.34) and control group (p < 0.05). There was no correlation between vitronectin and lipid parameters. CONCLUSION: These findings suggested that vitronectin is a marker of CAD. Elevated levels may indicate its role in the genesis and/or progression of CAD or may be the results of a compensatory mechanism.
Authors: P Dufourcq; H Louis; C Moreau; D Daret; M R Boisseau; J M Lamazière; J Bonnet Journal: Arterioscler Thromb Vasc Biol Date: 1998-02 Impact factor: 8.311
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