Abstract
Nitric oxide is a mediator of paracrine cell signalling. An inducible form of nitric oxide synthase (iNOS) is expressed in macrophages and in Swiss 3T3 cells. Transforming growth factor beta (TGF-beta) is a cytokine that modulates many cellular functions. We find that TGF-beta cannot induce iNOS mRNA expression, either in macrophage cell lines or in Swiss 3T3 cells. However, TGF-beta attenuates lipopolysaccharide induction of iNOS mRNA in macrophages. In contrast, TGF-beta enhances iNOS induction by phorbol ester, serum or lipopolysaccharide in 3T3 cells. Thus TGF-beta can inhibit or augment iNOS mRNA induction in response to primary inducers, depending on the cell type in question.
Publication types
- Research Support, U.S. Gov't, Non-P.H.S.
- Research Support, U.S. Gov't, P.H.S.
MeSH terms
- 3T3 Cells
- Amino Acid Oxidoreductases / biosynthesis*
- Amino Acid Oxidoreductases / genetics
- Animals
- Cell Line
- Dexamethasone / pharmacology
- Enzyme Induction / drug effects
- Gene Expression Regulation, Enzymologic / drug effects*
- Genes / drug effects
- Lipopolysaccharides / pharmacology
- Macrophages / enzymology*
- Mice
- Nitric Oxide Synthase
- RNA, Messenger / metabolism
- Transcription, Genetic / drug effects
- Transforming Growth Factor beta / pharmacology*
Substances
- Lipopolysaccharides
- RNA, Messenger
- Transforming Growth Factor beta
- Dexamethasone
- Nitric Oxide Synthase
- Amino Acid Oxidoreductases