Overexpression of redox factor‐1 negatively regulates NO synthesis and apoptosis in LPS‐stimulated RAW 264.7 macrophages

FEBS Letters

Park, Sang Eun¹  Park, Young Chul¹  Yoo, Young Hyun¹  Kim, Jong-Min¹  Lim, Young Jin² 

[1] Department of Anatomy and Cell Biology, Dong-A University College of Medicine (BK21 Program), Pusan 602-714, South Korea;Department of Parasitology, Dong-A University College of Medicine, Pusan 602-714, South Korea

关键词: Redox factor-1;    Nitric oxide;    Macrophage;    Lipopolysaccharide;    Apoptosis;    Ref-1;    redox factor-1;    NO;    nitric oxide;    iNOS;    inducible NO synthase;    LPS;    lipopolysaccharide;    ROS;    reactive oxygen species;   

DOI  :  10.1016/S0014-5793(03)01361-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Redox factor-1 (Ref-1) is a ubiquitously expressed protein with proven roles as a modulator of redox-sensitive transcription, and as an endonuclease in the base excision repair pathway of oxidatively damaged DNA. Although Ref-1 is induced by a variety of oxidative stress and protects cells against oxidative stress, the function of Ref-1 in regulating nitric oxide (NO) synthesis has not been elucidated to date. We investigated the role of Ref-1 in regulating NO synthesis and NO-mediated apoptosis employing adenoviral-mediated overexpression of Ref-1 in lipopolysaccharide (LPS)-stimulated macrophage RAW 264.7 cells. LPS treatment produced NO synthesis and NO-mediated apoptosis. Forced overexpression of Ref-1 suppressed LPS-stimulated NO synthesis. In parallel with this, Ref-1 also mitigated alteration of inducible NO synthase expression and NO-mediated apoptosis. Our findings suggest that Ref-1 is implicated in protection against cell death resulting from oxidative stimuli containing NO.

【 授权许可】

Unknown