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-γ), but not LPS. However, LPS augmented the NO production in IFN-γ-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-γ stimulation, accompanied by the delayed iNOS expression. The JAK/STAT signal pathway mediated IFN-γ-induced NO production, but did not participate in the LPS-induced augmentation. Further, no activation of nuclear factor (NF -κB was involved in the NO production in END-D cells stimulated with either IFN-γ 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.
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