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• W2143016221 abstract "Reactive oxygen species (ROS) play an important but not yet fully defined role in the expression of inflammatory genes such as monocyte chemoattractant protein (MCP)-1. We used complementary molecular and biochemical approaches to explore the roles of specific ROS and their molecular linkage to inflammatory signaling in endothelial cells. Adenovirus-mediated expression of superoxide dismutase and catalase inhibited TNF-α-induced MCP-1 gene expression, suggesting important roles of superoxide ([Formula: see text]) and H 2 O 2 in MCP-1 gene activation. In addition, the iron chelator 1,2-dimethyl-3-hydroxypyridin-4-one and the hydroxyl radical scavengers dimethylthiourea and dimethyl sulfoxide inhibited TNF-α-induced MCP-1 expression, suggesting important roles of iron and hydroxyl radicals in inflammatory signal activation. In contrast, scavenging of peroxynitrite with 5,10,15,20-tetrakis-(4-sulfonatophenyl)prophyrinato iron (III) chloride had no effect on TNF-α-induced MCP-1 expression. Inhibition of NADPH oxidase, the major oxidase responsible for [Formula: see text] generation, with diphenylene iodonium suppressed TNF-α-induced MCP-1 mRNA accumulation. Rac1 is an upstream signaling molecule for the activation of NADPH oxidase and [Formula: see text] generation. Expression of dominant negative N17Rac1 by adenovirus suppressed TNF-α-induced MCP-1 mRNA levels and MCP-1 protein secretion. Expression of N17Rac1 inhibited TNF-α-induced MCP-1 and NF-κB transcriptional activity. These data suggest that ROS such as superoxide and H 2 O 2 derived from Rac1-activated NADPH oxidase mediate TNF-α-induced MCP-1 expression in endothelial cells." @default.
• W2143016221 created "2016-06-24" @default.
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• W2143016221 date "2004-03-01" @default.
• W2143016221 modified "2023-10-15" @default.
• W2143016221 title "Superoxide, H₂O₂, and iron are required for TNF-α-induced MCP-1 gene expression in endothelial cells: role of Rac1 and NADPH oxidase" @default.
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• W2143016221 doi "https://doi.org/10.1152/ajpheart.00716.2003" @default.
• W2143016221 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14576080" @default.
• W2143016221 hasPublicationYear "2004" @default.
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