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Research Article Free access | 10.1172/JCI117842

Involvement of reactive oxygen intermediates in cyclooxygenase-2 expression induced by interleukin-1, tumor necrosis factor-alpha, and lipopolysaccharide.

L Feng, Y Xia, G E Garcia, D Hwang, and C B Wilson

Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.

Find articles by Feng, L. in: JCI | PubMed | Google Scholar

Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.

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Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.

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Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.

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Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.

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Published April 1, 1995 - More info

Published in Volume 95, Issue 4 on April 1, 1995
J Clin Invest. 1995;95(4):1669–1675. https://doi.org/10.1172/JCI117842.
© 1995 The American Society for Clinical Investigation
Published April 1, 1995 - Version history
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Abstract

Reactive oxygen intermediates (ROIs) play an important role in inflammatory processes as mediators of injury and potentially in signal transduction leading to gene expression. Cyclooxygenase (COX) is a rate-limiting enzyme in prostanoid biosynthesis, and its recently cloned inducible form, COX-2, is induced by proinflammatory cytokines. This study linked ROIs to the signaling pathways that induce COX-2 expression. The hydroxyl radical scavengers DMSO (1%), as well as di- and tetramethylthiourea, inhibited IL-1-, TNF alpha-, and LPS-induced COX-2 expression in rat mesangial cells. The suppression of COX-2 mRNA expression correlated with the COX-2 protein level. In comparison with the prolonged induction of the inducible gene encoding protein-tyrosine phosphatase by hydrogen peroxide, the COX-2 gene was only transiently induced. Protein-tyrosine phosphatase is also induced by heat shock and chemical stress, whereas COX-2 is not. Superoxide was a more potent inducer for COX-2 than hydrogen peroxide. In addition, NADPH stimulated COX-2 expression, and an inhibitor of NADPH oxidase blocked COX-2 expression induced by TNF alpha. COX-2 and KC gene expression costimulated by IL-1 were inhibited differentially by the scavengers. These studies demonstrate that oxidant stress is a specific and important inducer of COX-2 gene expression. This induction may contribute to the deleterious amplification of prostanoids in inflammation and compound the direct effects of ROI production.

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