Protein kinase C independent activation of inducible nitric oxide synthase by tumor necrosis factor-alpha in TM4 Sertoli cells

To investigate the nitric oxide (NO) production and its signalling mechanism in TM4 Sertoli cells, the cells were treated with recombinant tumor necrosis factor-alpha (rTNF-alpha), recombinant interleukin-1 alpha (rIL-1alpha), or lipopolysaccharide (LPS), either alone or in combination with recombin...

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Published inImmunopharmacology and immunotoxicology Vol. 22; no. 1; p. 49
Main Authors Chung, C K, Chung, B H, Shin, T, Chae, H J, Kim, H R, Cho, C C, Hong, G Y, An, N H, Kim, H M
Format Journal Article
LanguageEnglish
Published England 01.01.2000
Subjects
Animals
Blotting, Western
Cell Line
Enzyme Activation - drug effects
Enzyme Inhibitors
Interferon-gamma - pharmacology
Interleukin-1 - pharmacology
Lipopolysaccharides - pharmacology
Male
Mice
Nitric Oxide - biosynthesis
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Protein Kinase C - antagonists & inhibitors
Protein Kinase C - metabolism
Recombinant Proteins
Sertoli Cells - drug effects
Sertoli Cells - enzymology
Tumor Necrosis Factor-alpha - pharmacology
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Summary:To investigate the nitric oxide (NO) production and its signalling mechanism in TM4 Sertoli cells, the cells were treated with recombinant tumor necrosis factor-alpha (rTNF-alpha), recombinant interleukin-1 alpha (rIL-1alpha), or lipopolysaccharide (LPS), either alone or in combination with recombinant interferon-gamma (rIFN-gamma), and NO production was measured by using the Griess method. TM4 Sertoli cells produced a small amount of NO upon treatment with rIFN-gamma. The effect of rIFN-gamma was drastically increased by cotreatment with rTNF-alpha in a dose-dependent manner. However, combination of rIL-1alpha or LPS with rIFN-gamma did not synergize to activate cells. RIFN-gamma in combination with rTNF-alpha showed marked increase of the expression of iNOS protein. Protein kinase C inhibitors did not inhibit the production of NO induced by rIFN-gamma plus rTNF-alpha. These results suggest that the role of TNF-alpha is to provide TM4 Sertoli cells with the active cofactor for NO production and TNF-alpha-induced signaling for induction of NO synthesis is not dependent on protein kinase C activation.
ISSN:0892-3973
DOI:10.3109/08923970009016405