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

TitleCatalase induced expression of inflammatory mediators via activation of NF-kappaB, PI3K/AKT, p70S6K, and JNKs in BV2 microglia.
Publication TypeJournal Article
Year of Publication2005
AuthorsJang B-C, Paik J-H, Kim S-P, Shin D-H, Song D-K, Park J-G, Suh M-H, Park J-W, Suh S-I
JournalCell Signal
Volume17
Issue5
Pagination625-33
Date Published2005 May
ISSN0898-6568
KeywordsAnimals, Catalase, Cell Line, Cyclooxygenase 2, Enzyme Activation, Inflammation Mediators, JNK Mitogen-Activated Protein Kinases, Mice, Microglia, NF-kappa B, Nitric Oxide Synthase, Nitric Oxide Synthase Type II, Phosphatidylinositol 3-Kinases, Prostaglandin-Endoperoxide Synthases, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-akt, Ribosomal Protein S6 Kinases, 70-kDa, Signal Transduction, Sirolimus, Transcriptional Activation
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-kappaB, 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-kappaB 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.

DOI10.1016/j.cellsig.2004.10.001
Alternate JournalCell Signal
PubMed ID15683737
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Ji-Hye Paik, Ph.D.

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