Preliminary Study Showing the Relationship Between Platelet Fibronectin, Sialic Acid, and ADP-induced Aggregation Levels in Coronary Heart Disease

Abstract

Several studies indicate that thrombosis plays an important role in the pathogenesis of coronary heart disease (CHD). Fibronectin is a multifunctional protein in plasma, other body fluids, and cell surface and plays an important role in platelet functions, including mediation of cell-cell and cell-surface interactions. Sialic acid is a regular constituent of glycoproteins and gangliozides in the outer cell membrane of mammalian cells. Therefore, the sialic acid content of platelets, which are characterized by their ability to aggregate with each other, can be important in leading to thrombus formation. In this study, platelet fibronectin, sialic acid-, and adenosine diphosphate (ADP)-induced platelet aggregation levels were determined in patients with CHD. Platelet sialic acid concentrations were determined by Warren's method. Platelet aggregation tests with ADP in platelet-rich plasma (PRP) were analyzed by use of an aggregometer. Platelet homogenate fibronectin levels were determined by ELISA. Total protein levels were determined by Lowry method. Our results indicate that, in patients with no vessel disease (patients with no obstructed vessel but suffering from chest pain, like angina pectoris) platelet fibronectin levels were significantly lower than the total of the other patients (patients with 1, 2, or 3 obstructed coronary vessels) (p<0.05). Sialic acid levels in patients with no vessel disease were significantly lower than the total of the patient group (p<0.05). There was significant (+) correlation between platelet aggregation, platelet fibronectin, platelet sialic acid, and severity of disease (p<0.05). Our preliminary findings suggest that, especially platelet fibronectin levels potentially represent a pathogenic factor for CHD.

Desialylation is a mechanism of Fc-independent platelet clearance and a therapeutic target in immune thrombocytopenia

“…These findings also provide insights into the platelet activation–desialylation dialogue and its positive feedback loop, which may contribute to thrombosis and cardiovascular diseases. Platelet activation and desialylation have been previously described in coronary heart disease (CHD) patients 67 68 , in which the sialic content of platelets was inversely correlated with the severity of CHD 67 . In addition, compared with patients without CHD, CHD patients overall exhibited more desialylated platelets that were prone to aggregation with higher sensitivity to weak agonists, such as ADP and serotonin 68 69 .…”

“…Platelet activation and desialylation have been previously described in coronary heart disease (CHD) patients 67 68 , in which the sialic content of platelets was inversely correlated with the severity of CHD 67 . In addition, compared with patients without CHD, CHD patients overall exhibited more desialylated platelets that were prone to aggregation with higher sensitivity to weak agonists, such as ADP and serotonin 68 69 . These reports strongly reinforce the notion that platelet desialylation potentiates activation of platelets in other disease states, which may result in aggregation and platelet consumption.…”