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.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology
- Infectious Diseases