INHIBITION BY LYSOPHOSPHATIDYLCHOLINE OF NITRIC OXIDE PRODUCTION IN INTERLEUKIN 1β-STIMULATED : VASCULAR SMOOTH MUSCLE CELLS

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In vascular smooth muscle cells (VSMC), inflammatory cytokines such as interleukin 1 beta(IL-1 beta) stimulated nitric oxide (NO) production via the expression of an inducible type of NO synthase (iNOS). Lysophosphatidylcholine (LPC) is a major phospholipid component of atherogenic oxidized low density lipoprotein (Ox-LDL). In this study, we examined the effect of LPC on IL-1 beta-stimulated NO production in cultured. VSMC. LPC by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose-dependently inhibited IL-1 beta-stimulated nitrite production. LPC inhibited IL-1 beta-stimulated iNOS protein expression, whereas LPC did not inhibit IL-1 beta-stimulated iNOS mRNA expression. Analysis of iNOS protein degradation rate revealed that LPC had no effect on degradation rate of iNOS protein, suggesting that LPC inhibited iNOS translation. Moreover, Ox-LDL inhibited IL-1 beta-stimulated NO production by inhibiting iNOS protein expression without affecting iNOS mRNA expression. These results indicate that Ox-LDL negatively modulates IL-1 beta-induced NO production through the action of LPC, probably by blocking translation of iNOS mRNA.
神戸大学の論文