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Differences in the mechanism of nitric oxide production between mouse vascular endothelial cells and macrophages

Department of Microbiology and Immunology, and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan, sugiyama{at}aichi-med-u.ac.jp

Megumi Fujita

Department of Public Health Pharmacy, Gifu Pharmaceutical University, Gifu, Japan

Naoki Koide

Department of Microbiology and Immunology, and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Akiko Morikawa

Department of Microbiology and Immunology, and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Kazuko Takahashi

Department of Microbiology and Immunology, and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Tomoaki Yoshida

Department of Microbiology and Immunology, and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Hiroshi Mori

Department of Public Health Pharmacy, Gifu Pharmaceutical University, Gifu, Japan

Takashi Yokochi

Department of Microbiology and Immunology, and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

The detailed mechanism of NO production in mouse vascular endothelial cells, END-D, was studied. The NO production in END-D cells was triggered by gamma interferon (IFN-), but not LPS. However, LPS augmented the NO production in IFN--stimulated END-D cells. A high level of NO production was due to the expression of an inducible type of NO synthase (iNOS) in those cells. A significant amount of NO was detected 18 h after IFN- stimulation, accompanied by the delayed iNOS expression. The JAK/STAT signal pathway mediated IFN--induced NO production, but did not participate in the LPS-induced augmentation. Further, no activation of nuclear factor (NF)-B was involved in the NO production in END-D cells stimulated with either IFN- and/or LPS. The mechanism of NO production in END-D cells was suggested to be different from that in mouse macrophages. The differential regulation of NO production in mouse vascular endothelial cells and macrophages is discussed.

Journal of Endotoxin Research, Vol. 9, No. 2, 108-112 (2003)
DOI: 10.1177/09680519030090020601


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