scholarly journals Insulin inhibits inducible nitric oxide synthase in skeletal muscle cells

Diabetologia ◽  
1998 ◽  
Vol 41 (12) ◽  
pp. 1523-1527 ◽  
Author(s):  
S. Bédard ◽  
B. Marcotte ◽  
A. Marette
2005 ◽  
Vol 280 (14) ◽  
pp. 14203-14211 ◽  
Author(s):  
Hiroki Sugita ◽  
Masaki Fujimoto ◽  
Takashi Yasukawa ◽  
Nobuyuki Shimizu ◽  
Michiko Sugita ◽  
...  

1997 ◽  
Vol 272 (1) ◽  
pp. C35-C40 ◽  
Author(s):  
S. Okuda ◽  
F. Kanda ◽  
Y. Kawahara ◽  
K. Chihara

Cytokine-stimulated expression of inducible type of nitric oxide synthase (iNOS) seems to be regulated by various signal pathways in a cell-specific manner. In this study, we examined how it was regulated in L6 rat skeletal muscle cells. In L6 cells, the combination of interleukin-1 beta and interferon-gamma induced a marked accumulation of nitrite, a stable metabolite of nitric oxide. In parallel with this reaction, iNOS mRNA expression was achieved at a maximum between 3 and 6 h, and iNOS protein was detectable at 6 h and peaked at 24 h after stimulation. Tyrosine kinase inhibitors, herbimycin A, and genistein suppressed cytokine-induced iNOS expression and nitrite production. Forskolin, an adenosine 3',5'-cyclic monophosphate-dependent protein kinase (PKA) activator, and phorbol 12-myristate 13-acetate, a protein kinase C (PKC)-activating phorbol ester, enhanced these cytokine-induced reactions. These results indicate that iNOS expression by cytokines is mediated via a protein tyrosine kinase-dependent pathway and is positively modulated by both PKA- and PKC-dependent pathways in this cell type.


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