Premium
Overexpression of redox factor‐1 negatively regulates NO synthesis and apoptosis in LPS‐stimulated RAW 264.7 macrophages
Author(s) -
Yoo Young Hyun,
Lim Young Jin,
Park Sang Eun,
Kim Jong-Min,
Park Young Chul
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01361-9
Subject(s) - apoptosis , oxidative stress , microbiology and biotechnology , chemistry , transcription factor , lipopolysaccharide , nitric oxide , transcription (linguistics) , programmed cell death , oxidative phosphorylation , biology , biochemistry , gene , immunology , linguistics , philosophy , organic chemistry
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.