Patterns and levels of platelet glycosylation in patients with coronary heart disease and type 2 diabetes mellitus

Coronary heart disease (CHD) and diabetes mellitus (DM) have high reactivity of platelets and an increased risk of thrombosis. Platelet glycosylation is closely related to platelet function and survival. However, the alteration of platelet glycosylation in CHD and T2DM still remains unknown. Platelet samples were obtained from 55 healthy controls and 102 patients, including 33 CHD, 30 T2DM and 39 CHD complicated with T2DM (CHD + T2DM). Platelet glycosylation was detected using eight-lectin based assay by flow cytometry. Platelet activation markers, such as CD62P (P-Selectin) and activated integrin GPIIb/IIIa (PAC-1), were measured on resting and stimulated conditions by flow cytometry. Platelet aggregation was measured by light transmission aggregometry. In CHD group, platelet surface weakly expressed β-Gal and 2,6-sialic acid and strongly expressed β-GlcNAc. In T2DM group, lectins binding to platelet of β-Gal, 2,6-sialic acid and α-mannose were decreased, while α1,6-fucose and GlcNAc were increased. There was positive correlation between ConA (specific for α-mannose) and PAC-1 in T2DM patients, while negative correlation in healthy controls. Patterns and levels of platelet glycosylation in CHD + T2DM group are a combination of CHD group and T2DM group, in addition to the level of ECL highly elevated (specific for β-Gal). The level of ConA was significantly correlated with glucose in T2DM group, also correlated with HbA1c in CHD + T2DM. Our findings suggested that platelets decreased in sialylation, galactosylation and mannosylation, and increased in fucosylation and GlcNAcylation in CHD and T2DM patients. The changes of platelet glycosylation may be associated with high platelet reactivity and the increased risk of thrombosis in CHD and T2DM.