|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
2
|
|
pubmed:dateCreated |
2003-6-13
|
|
pubmed:abstractText |
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-gamma), but not LPS. However, LPS augmented the NO production in IFN-gamma-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-gamma stimulation, accompanied by the delayed iNOS expression. The JAK/STAT signal pathway mediated IFN-gamma-induced NO production, but did not participate in the LPS-induced augmentation. Further, no activation of nuclear factor (NF)-kappaB was involved in the NO production in END-D cells stimulated with either IFN-gamma 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.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Jak1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Janus Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/STAT2 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
|
|
pubmed:status |
MEDLINE
|
|
pubmed:issn |
0968-0519
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
9
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
108-12
|
|
pubmed:dateRevised |
2009-11-19
|
|
pubmed:meshHeading |
pubmed-meshheading:12803884-Animals,
pubmed-meshheading:12803884-Cell Line,
pubmed-meshheading:12803884-DNA-Binding Proteins,
pubmed-meshheading:12803884-Dose-Response Relationship, Drug,
pubmed-meshheading:12803884-Endothelium, Vascular,
pubmed-meshheading:12803884-Escherichia coli,
pubmed-meshheading:12803884-Interferon-gamma,
pubmed-meshheading:12803884-Janus Kinase 1,
pubmed-meshheading:12803884-Lipopolysaccharides,
pubmed-meshheading:12803884-Macrophages,
pubmed-meshheading:12803884-Mice,
pubmed-meshheading:12803884-Nitric Oxide,
pubmed-meshheading:12803884-Nitric Oxide Synthase,
pubmed-meshheading:12803884-Nitric Oxide Synthase Type II,
pubmed-meshheading:12803884-Protein-Tyrosine Kinases,
pubmed-meshheading:12803884-STAT2 Transcription Factor,
pubmed-meshheading:12803884-Signal Transduction,
pubmed-meshheading:12803884-Trans-Activators
|
|
pubmed:year |
2003
|
|
pubmed:articleTitle |
Differences in the mechanism of nitric oxide production between mouse vascular endothelial cells and macrophages.
|
|
pubmed:affiliation |
Department of Microbiology and Immunology, and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan. sugiyama@aichi-med-u.ac.jp
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
