Sulfatides are associated with neointimal thickening after vascular injury.
ABSTRACT Sulfatides are known to be a native ligand of P-selectin. Platelet-leukocyte interaction via the cross-talk between P-selectin and Mac-1 (CD11b/CD18) plays an important role in the mechanism of neointimal thickening after vascular injury such as that seen in post-stent restenosis. However, the roles of sulfatides on restenosis have not been elucidated.
Serum sulfatide levels, P-selectin expression on the surface of platelets, and activated Mac-1 on the surface of neutrophils were serially measured using both coronary sinus and peripheral blood samples in 21 patients who underwent coronary stent implantation.
The trans-cardiac gradient (coronary sinus minus peripheral blood) of the sulfatide levels significantly increased at 15 min (-1.47+/-2.87 to 0.59+/-1.44 nmol/ml, p<0.001), compared to baseline levels. The maximum response of the trans-cardiac gradient of P-selectin expression on the surface of platelets at 15 min after stent implantation (R=0.55, p<0.01), and that of activated Mac-1 on the surface of neutrophils at 48 h (R=0.59, p<0.01), were both positively correlated with that of serum sulfatide levels at 15 min. The angiographic late lumen loss was correlated with the trans-cardiac gradient of sulfatide levels at 15 min (R=0.48, p<0.05), platelet P-selectin expression at 15 min (R=0.42, p<0.05) and activated neutrophil Mac-1 expression at 48 h (R=0.46, p<0.05), but not with values at other sampling points.
Sulfatides may play a physiological role on inflammation in vascular injury and the development of neointimal thickening.
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ABSTRACT: There is a positive association between sulfatide and atherosclerosis in an animal model for human familial hypercholesterolemia. Carotid intima-media thickness (IMT) is thought to be a marker of atherosclerosis in humans. We investigated the relationship between sulfatide and carotid IMT in heterozygous familial hypercholesterolemia (FH) patients. Thirty-five genetically-verified heterozygous patients with FH and 34 healthy controls were recruited into our study. We measured serum sulfatide levels, the carotid IMT, and conventional cardiovascular risk factors including obesity parameters, blood pressure, fasting blood glucose, and lipid profiles. Subjects with heterozygous FH had significantly elevated serum sulfatide, elevated total cholesterol, low-density lipoprotein cholesterol, and increased carotid IMT compared with control subjects. In patients with FH, univariate analysis showed that serum sulfatide was significantly correlated with carotid IMT. Multiple linear regression analysis indicated that serum sulfatide was the only independent predictor of carotid IMT in patients with FH. Patients with heterozygous FH had significantly higher carotid IMT and the level of serum sulfatide was independently associated with atherosclerotic progression. (R: 0.720, R(2): 0.503, p < 0.001).Glycoconjugate Journal 08/2014; 31(8). · 1.88 Impact Factor
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ABSTRACT: In this paper, we focus our study to follow systematically the influence of the magnetic field on the crystal form of calcium carbonate precipitated from low-concentration water solutions. By changing the strength of the field and the flow rate of the water through the system the calcite/aragonite/vaterite ratio varied. The crystal form and the particle size distribution of the precipitated calcium carbonate were determined by using X-ray analysis and HREM. The theoretical part of the work was to study the mechanism of the influence of magnetic field on the nucleation and further crystallisation of calcium carbonate. Starting from ab-initio calculations scaling can be explained easily on the basis of shape and energy position of the ground electronic states of calcite and aragonite.01/2003;
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ABSTRACT: Sulfatides are sphingolipids commonly found at the surface of most of eukaryotic cells. Sulfatides are not just structural components of the plasma membrane but also participate in a wide range of cellular processes including protein trafficking, cell adhesion and aggregation, axon-myelin interactions, neural plasticity, and immune responses, among others. The intriguing question is how can sulfatides trigger such cellular processes? Their dynamic presence and specific localization at plasma membrane sites may explain their multitasking role. Crystal and NMR structural studies have provided the basis for understanding the mechanism of binding by sulfatide-interacting proteins. These proteins generally exhibit a hydrophobic cavity that is responsible for the interaction with the sulfatide acyl chain, whereas the hydrophilic, negatively charged moiety can be found either buried in the hydrophobic cavity of the protein or exposed for additional intermolecular associations. Since sulfatides vary in their acyl chain composition, which are tissue-dependent, more emphasis on understanding acyl chain specificity by sulfatide-binding proteins is warranted. Importantly, changes in cellular sulfatide levels as well as circulating sulfatides in serum directly impact cardiovascular and cancer disease development and progress. Therefore, sulfatides might prove useful as novel biomarkers. The scope of this review is to overview cell functions and mechanisms of sulfatide recognition to better understand the role of these lipids in health and disease.Advances in Experimental Medicine and Biology 01/2013; 991:27-40. · 2.01 Impact Factor