Sulfatides are associated with neointimal thickening after vascular injury.

Department of Cardiovascular Medicine, Dokkyo Medical University, 880 Kitakobayashi, Mibu, Tochigi, 321-0293 Japan.
Atherosclerosis (Impact Factor: 3.71). 02/2010; 211(1):291-6. DOI: 10.1016/j.atherosclerosis.2010.01.033
Source: PubMed

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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