p38 Mitogen-Activated Protein Kinase and Extracellular Signal-Regulated Kinase Regulate Nitric Oxide Production and Inflammatory Cytokine Expression in Raw Cells
Immune Network
; : 30-35, 2005.
Article
in English
| WPRIM (Western Pacific)
| ID: wpr-127002
Responsible library:
WPRO
ABSTRACT
BACKGROUND:
p38 and extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) signaling are thought to have critical role in lipopolysaccharide (LPS)-induced immune response but the molecular mechanism underlying the induction of these signaling are not clear.METHODS:
Specific inhibitors for p38, SB203580, and for ERK, PD98059 were used. Cells were stimulated by LPS with or without specific MAPK inhibitors.RESULTS:
LPS activated inducible nitric oxide synthase (iNOS), subsequent NO productions, and pro-inflammatory cytokine gene expressions (TNF-alpha, IL-1beta, IL-6, and IL-12). Treatment of both SB203580 and PD98059 decreased LPS-induced NO productions. Concomitant decreases in the expression of iNOS mRNA and protein were detected. SB203580 and PD98059 decreased LPS-induced gene expression of IL-1beta and IL-6. SB203580 increased LPS-induced expression of TNF-alpha and IL-12, and reactive oxygen species production, but PD98059 had no effect.CONCLUSION:
These results indicate that both p38 and ERK pathways are involved in LPS-stimulated NO synthesis, and expression of IL-1beta and IL-6. p38 signaling pathways are involved in LPS-induced TNF-alpha and IL-12, and reactive oxygen species plays an important role in these signaling in macrophage.
Full text:
Available
Database:
WPRIM (Western Pacific)
Main subject:
Phosphotransferases
/
Protein Kinases
/
RNA, Messenger
/
Gene Expression
/
Interleukin-6
/
Tumor Necrosis Factor-alpha
/
Reactive Oxygen Species
/
Interleukin-12
/
MAP Kinase Signaling System
/
Nitric Oxide Synthase Type II
Language:
English
Journal:
Immune Network
Year:
2005
Document type:
Article