Kobe Journal of Medical Sciences, 1998

sI: Inhibition by lysophosphatidylcholine of nitric oxide production in interleukin 1 beta-stimulated vascular smooth muscle cells.

AU: Okamoto-Y; Kawahara-Y; Yokoyama-M

AD: Department of Internal Medicine, Kobe University School of Medicine.

SO: Kobe-J-Med-Sci. 1998 Aug; 44(4): 169-89

ISSN: 0023-2513

PY: 1998



AB: 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.

Published Bimonthly by Kobe University School of Medicine, Kobe, Japan