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Changes in sialylation of low‐density lipoprotein in coronary artery disease
Author(s) -
Goodarzi Mohammad Taghi,
Rezaei Mohsen,
Moadel Esmaeil,
Homayounfar Shahram,
Safari Mohammad Reza
Publication year - 2008
Publication title -
european journal of lipid science and technology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 94
eISSN - 1438-9312
pISSN - 1438-7697
DOI - 10.1002/ejlt.200700189
Subject(s) - sialic acid , coronary artery disease , pathogenesis , medicine , low density lipoprotein , chemistry , cad , lipoprotein , glycosylation , endocrinology , biochemistry , cholesterol
Reduction of LDL sialylation may correlate with coronary artery disease (CAD), but the details of this modification and its effect on CAD are not well studied. This study was aimed to show desialylation of LDL and to reveal more details of this modification. Blood samples were collected from 16 patients with CAD and 25 healthy individuals. Serum sialic acid was determined. LDL was extracted from all samples, and the interaction of the extracted materials with lectins (MAA, SNA, and DSA) was studied using the lectin blotting method. Serum total sialic acid (TSA) concentrations in CAD patients and healthy individuals were 71.9 ± 2.66 and 60.76 ± 2.34 mg/dL, respectively, and the difference between the two groups was statistically significant ( p <0.001). The intensity of interaction of extracted LDL with SNA and MAA lectins was lower in CAD patients compared to that in normal subjects ( p <0.001). The intensity of interaction of LDL with DSA was higher in CAD ( p <0.001). There was a reverse correlation between TSA and intensity of LDL interaction with SNA and MAA in both groups, but in the case of DSA this correlation was direct and positive. These findings indicated an increase in desialylation of LDL in CAD. It was concluded that LDL was subjected to glycosylation changes in CAD and that there was a positive correlation between TSA and the desialylated form of LDL. This modification may contribute to the pathogenesis of CAD.