Phosphatidylinositol-3-kinase Inhibitor Enhances Nitric Oxide Synthesis and Apoptosis in LPS-Stimulated Macrophages.
- Author:
Young Chul PARK
1
Author Information
1. Department of Anatomy and Cell Biology (BK21 Program), Dong-A University College of Medicine, Pusan 602-714, Korea. parkyc@daunet.donga.ac.kr
- Publication Type:Original Article
- Keywords:
Macrophage;
PI3-kinase;
LPS;
NO;
Apoptosis
- MeSH:
Apoptosis*;
Cell Proliferation;
Macrophage Activation;
Macrophages*;
Nitric Oxide Synthase;
Nitric Oxide*;
Phosphatidylinositol 3-Kinases
- From:Korean Journal of Anatomy
2003;36(4):323-329
- CountryRepublic of Korea
- Language:English
-
Abstract:
Phosphatidylinositol-3-kinase (PI3-kinase) is critical player in cell proliferation and death. The mechanism by which bacterial lipopolysaccharide (LPS) induces synthesis of nitric oxide (NO) in murine macrophages is incompletely understood. In this study we examined the effects of wortmannin and LY294002, two inhibitors of PI3-kinase, on the induction of NO synthesis and NO-mediated apoptosis in LPS-stimulated macrophages. Treatment of wortmannin and LY294002 markedly potentiated NO synthesis and inducible NO synthase (iNOS) expression in LPS-stimulated cells. Furthermore, wortmannin also enhanced apoptosis in LPS-stimulated cells. These results suggest that PI3-kinase might play an important role in transducing the signal that involved in LPS-induced macrophage activation.
