NDLI: Exogenous Nitric Oxide Inhibits Tumor Necrosis Factor-Alpha- or Interleukin-1-Beta-Induced Monocyte Chemoattractant Protein-1 Expression in Human Mesangial Cells

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Exogenous Nitric Oxide Inhibits Tumor Necrosis Factor-Alpha- or Interleukin-1-Beta-Induced Monocyte Chemoattractant Protein-1 Expression in Human Mesangial Cells

Content Provider	Semantic Scholar
Author	Lee, Sang Koo Kim, Cheol Su Yang, Won Seok Kim, Soon Bae Park, Sun Cheol Park, Jung Sik
Copyright Year	2002
Abstract	Monocyte chemoattractant protein-1 (MCP-1) plays an important role in glomerulonephritis and nitric oxide (NO) exerts a variety of renal pathophysiological effects. We investigated the effect of exogenous NO on pro-inflammatory cytokine-induced MCP-1 expression in human mesangial cells and its signal transduction pathway. Cells were pretreated with NO donors such as 3-morpholino-sydnonimine (SIN-1) or nitroprusside, and then stimulated with tumor necrosis factor-α (TNF-α) or interleukin-1β (IL-1β). MCP-1 expression of mRNA and protein were measured by Northern blot analysis and ELISA. NF-ĸB binding activity was determined by electrophoretic mobility shift assay. Degradation of IĸB-α protein was assessed by Western blot analysis. SIN-1 inhibited TNF-α- or IL-1β-induced MCP-1 mRNA expression in a dose-dependent manner and also suppressed the MCP-1 protein expression. Nitroprusside inhibited the MCP-1 mRNA expression as well. SIN-1 dose dependently inhibited the TNF-α- or IL-1β-induced NF-ĸB binding activity and suppressed the TNF-α-induced degradation of IĸB-α. Analogue of cGMP (8-bromo-cGMP) had no significant effect on TNF-α-induced MCP-1 mRNA expression and guanylate cyclase inhibitor (ODQ) also had no significant influence on the inhibitory effect of SIN-1. These results suggest that exogenous NO inhibits MCP-1 expression via suppression of NF-ĸB by reducing the degradation of IĸB-α and through a cGMP-independent pathway.
Starting Page	780
Ending Page	787
Page Count	8
File Format	PDF HTM / HTML
DOI	10.1159/000065441
Volume Number	92
Alternate Webpage(s)	https://www.karger.com/Article/Pdf/65441
Alternate Webpage(s)	https://doi.org/10.1159/000065441
Journal	Nephron
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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