계명대학교 의학도서관 Repository

Catalase induced expression of inflammatory mediators via activation of NF-κB, PI3K/AKT, p70S6K, and JNKs in BV2 microglia

Metadata Downloads
Author(s)
장병철박종구김상표신동훈송대규박종욱서성일서민호
Alternative Author(s)
Jang, Byeong ChurlPark, Jong GuKim, Sang PyoShin, Dong HoonSong, Dae KyuSuh, Min HoPark, Jong WookSuh, Seong Il
Publication Year
2005
Abstract
Catalase induces COX-2 or iNOS expression in some type of cells, but the mechanism remains unclear. Here we investigated the effect of catalase on COX-2 and iNOS expression in BV2 microglia and the inductive mechanism associated. Exposure of catalase to BV2 microglia induced expression of COX-2 and iNOS that was related with transcriptional up-regulation. Importantly, catalase-induced COX-2 and iNOS expression needed activations of NF-κB, PI3K/AKT, and JNKs, which were important for the transcriptional up-regulation of COX-2 and iNOS. Notably, rapamycin inhibition of p70S6K led to down-regulation of COX-2 and iNOS protein expression, but not steady-state mRNA expression and transcription, induced by catalase, suggesting that p70S6K is involved in increased COX-2 and iNOS mRNA translation by catalase. Interestingly, there was PI3K-dependent activation of AKT, p70S6K, JNKs, and NF-κB in response to catalase. These data collectively suggest catalase-induced COX-2 and iNOS expression in BV2 microglia is, in part at least, mediated through activation of multiple signaling proteins.

Abbreviations
AT, 3-amino-1,2,4-triazole;
ERKs, extracellular-regulated protein kinases;
GAPDH, glyceraldehyde 3-phosphate dehydrogenase;
iNOS, inducible nitric oxide synthase;
IκB, inhibitory kappa B;
JNKs, c-Jun N-terminal kinases;
NF-IL6, nuclear factor-interleukin 6;
NF-κB, nuclear factor-kappa B;
NO, nitric oxide;
PGs, prostaglandins;
PI3K, phosphatidylinositol 3 kinase;
ROS, reactive oxygen species

Keywords
Catalase;
Microglia;
COX-2;
iNOS;
JNK;
NF-κB;
PI3K/AKT/p70S6K
Authorize & License
  • AuthorizeOpen
  • EmbargoForever
Files in This Item:

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.