Visit our Expo - Redox and Inflammation signaling 2012

Session XIV : Transcriptional and translational control Poster XIV, 14
Signal transduction on the expression of inflammatory enzymes in Helicobacter pylori -
infected gastric epithelial cells
Soon Ok Cho, Hyeyoung Kim, Kyung Hwan Kim
Department of Pharmacology and Brain Korea 21 Project for Medical Science
Yonsei University College of Medicine, Seoul 120-752, Korea
E-mail:ehrehrwh@hanmail.net
Cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) are important
enzymes that mediate inflammatory processes. Oxygen radicals are important regulators in
Helicobacter pylori (H. pylori)-induced gastric ulceration and carcinogenesis, COX-2 and
iNOS may be regulated by oxidant-sensitive transcription factors, NF-kB and AP-1. In
addition, the binding sites for NF-kB and AP-1 are found in the promoter region of COX-2
and iNOS gene. Present study aims to investigate whether H. pylori-induced expressions of
COX-2 and iNOS are regulated by NF-kB and AP-1 in gastric epithelial AGS cells, and
whether the transcriptional regulation of COX-2 and iNOS are inhibited by transfection with
mutant genes for Ras (ras N-17), c-jun (TAM67), and IkBa (MAD3). As a result, H. pylori
induced the expression of mRNA and protein for COX-2 and iNOS via activation of NF-kB
and AP-1. Transfection with mutant genes for Ras (ras N-17), c-jun (TAM67), and IkBa
(MAD3) inhibited H. pylori-induced COX-2 and iNOS expression in AGS cells. In
conclusion, H. pylori induced activation NF-kB and AP-1 and thus COX-2 and iNOS
expression in gastric epithelial cells. Either suppression of NF-kB or AP-1 may inhibit H.
pylori-induced COX-2 and iNOS expression in gastric epithelial cells.
- 517 -