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J. Biochem, 2001, Vol. 129, No. 1 77-86
© 2001 Japanese Biochemical Society

other

Octamer Binding Protein-1 Is Involved in Inhibition of Inducible Nitric Oxide Synthase Expression by Exogenous Nitric Oxide in Murine Liver Cells1

Bok-Soo Lee, Yong-Man Kim, Hyung-Sik Kang, Hwan Mook Kim, Kwang-Ho Pyun and Inpyo Choi2

Laboratory of Immunology, Korea Research Institute of Bioscience and Biotechnology, Yusong Taejon 305-333, Republic of Korea

2To whom correspondence should be addressed. Tel: +82-42-860-4223, Fax: +82-42-860-4593, E-mail: ipchoi{at}kribb4680.kribb.re.kr

Nitric oxide (NO) has diverse effects on immune responses and hepatic functions. In BNL CL.2 cells, the murine embryonic liver cells, inducible nitric oxide synthase (iNOS) mRNA expression appeared after 3 h of treatment with IFN-{gamma} and LPS. Interestingly, mRNA and protein expression of iNOS was down-regulated by sodium nitroprusside (SNP) and diethylamine dinitric oxide in a time- and dose-dependent manner, but not by H2O2. TNF-{alpha} gene expression was also dramatically reduced by SNP, but IL-6 gene expression was inhibited much less. IFN-{gamma} and LPS-induced chloramphenicol acetyl-transferase activity of iNOS promoter constructs was inhibited by SNP. Electrophoretic mobility shift assay showed that SNP inhibited IFN-{gamma} plus LPS-induced Oct-1 binding activity, and the inhibition was reversed by DTT. Mutation in the Oct-1 site completely abolished iNOS promoter activity. In addition, supershift assay and Southwestern analysis demonstrated that the Oct-1 binding activity was inhibited by SNP. Taken together, these results indicate that NO suppresses IFN-{gamma} plus LPS-induced iNOS expression, and that Oct-1 is an important element in this process.

1This work was supported by grants (HAN project HS2620 and KG1511) from MOST, Republic of Korea.


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