Regular ArticleNitric Oxide Regulation of IL-8 Expression in Human Endothelial Cells
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Activation of eNOS in endothelial cells exposed to ionizing radiation involves components of the DNA damage response pathway
2015, Biochemical and Biophysical Research CommunicationsChanges in inflammatory gene expression induced by hyperbaric oxygen treatment in human endothelial cells under chronic wound conditions
2012, Experimental Cell ResearchCitation Excerpt :A number of studies have provided evidence linking ˙NO production to the regulation of IL-8. An early study suggested that treatment of endothelial cells with ˙NO inhibitors or ˙NO donors decreased or increased IL-8 levels, respectively [23]. However, our own data suggest that increased eNOS expression correlates with reduced IL-8 expression at the mRNA level and protein level in endothelial cells treated with HBO.
Current theories on the pathophysiology of multiple organ failure after trauma
2010, InjuryCitation Excerpt :It has been suggested that low levels NO derived from nNOS and eNOS is beneficial, whereas large amounts of iNOS-derived NO is harmful and contributes to tissue damage.55 In vitro studies have found that NO up-regulates the production of pro-inflammatory cytokines (TNF-α, IL-8 and prostaglandins) in LPS-stimulated human whole blood,97 LPS-stimulated murine macrophage cell line19 and TNF-α-stimulated human endothelial cell lines.96 In animal studies, several investigators have demonstrated that the expression of iNOS reached significant levels during haemorrhagic shock, which lead to tissue injury of lung, liver42,90,96 and intestine.43
Nitric oxide utilizes NF-κB to signal its neuroprotective effect against alcohol toxicity
2009, NeuropharmacologyCitation Excerpt :DETA-NONOate activates sGC by serving as an NO donor. 1.0 mM DETA-NONOate was used because it releases substantial NO quantities without evident toxicity (Villarete and Remick, 1995). 8-Br-cGMP is a cGMP analog that activates the NO–cGMP–PKG pathway by stimulating PKG.