Lipoprotein(a) enhances the expression of intercellular adhesion molecule-1 in cultured human umbilical vein endothelial cells

Article

关键词: LOW-DENSITY-LIPOPROTEIN;    CORONARY HEART-DISEASE;    HUMAN-PLASMA;    LP(A) LIPOPROTEIN;    HUMAN-MONOCYTES;    ATHEROGENESIS;    PLASMINOGEN;    LYMPHOCYTES;    INFARCTION;    ACTIVATION;   

DOI  :  10.1161/01.CIR.97.8.721

来源: SCIE

【 摘 要 】

Background-We reported an increase in serum lipoprotein(a) [Lp(a)] levels in patients with thromboangiitis obliterans, suggesting that Lp(a) could also contribute to the pathogenesis of cardiovascular diseases by a mechanism different from atherosclerosis. Adhesion molecules were shown to contribute to the development of not only atherosclerotic but also inflammatory vascular diseases, Methods and Results-We evaluated the effect of Lp(a) on the expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, and E-selectin in human umbilical vein endothelial cells by a cell ELISA. Lp(a) dramatically enhanced the levels of ICAM-1 in a dose-dependent manner. A discernible increase ill ICAM-1 expression was observed at a physiological concentration of 0.26 mmol cholesterol/L Lp(a) after 48-hour incubation. A 1.8-fold increase in ICAM-1 expression was observed 46 hours after the addition of Lp(a) (1.04 mmol cholesterol/L), Northern blot analysis demonstrated that the amount of ICAM-1 mRNA was increased after treatment with Lp(a), III contrast to ICAM-1, the expression of VCAM-1 and E-selectin was not significantly affected by Lp(a). Lp(a-) [apolipoprotein(a)-removed Lp(a) by reduction with dithiothreitol] and LDL had no significant effect on the expression of ICAM-1, In contrast, recombinant apolipoprotein(a) protein alone significantly enhanced ICAM-1 expression, Lp(a) decreased the level of active transforming growth factor (TGF)-beta in the conditioned medium. Furthermore, recombinant TGF-beta significantly decreased the Lp(a)-induced ICAM-1 expression, These findings suggested that Lp(a) may enhance the ICAM-1 expression by decreasing active TGF-beta level. Conclusions-Lp(a) could contribute to the development of cardiovascular diseases by enhancing the expression of ICAM-1 in endothelial cells.

【 授权许可】

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