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JCI table of contents: September 21, 2006

e at: https://www.the-jci.org/article.php?id=27643


INFLAMMATION: Platelets do the two-step to activate COX2

Chronic inflammation is a feature of many diseases, including heart disease and rheumatoid arthritis. One protein whose overexpression is thought to have a crucial role in maintaining the chronic inflammatory state is cyclooxygenase 2 (COX2). However, the mechanisms regulating COX2 expression have not been well defined. Now, in a study appearing online on September 21 in advance of publication in the October print issue of the Journal of Clinical Investigation, Dan Dixon and colleagues from the University of South Carolina, have shown that in human cells COX2 expression is controlled by a two-step process. The first step is controlled directly by interactions between monocytes (a type of inflammatory cell) and activated platelets, which activate expression of the COX2 gene. The second step is also initiated by interactions between monocytes and activated platelets but it is indirect: activated platelets induce monocytes to produce a soluble factor known as IL-1-beta, which then acts on the monocytes to enable them to produce COX2 protein. Because COX2 is overexpressed in chronic inflammatory conditions, the authors suggest that one, or both, of these two control steps might be dysregulated in disease.

TITLE: Expression of COX-2 in platelet-monocyte interactions occurs via combinatorial regulation involving adhesion and cytokine signaling

AUTHOR CONTACT: Dan A. Dixon University of South Carolina, Columbia, South Carolina, USA. Phone: (803) 434-3713; Fax: (803) 434-3795; E-mail: ddixon@biol.sc.edu.

Adam Cohen Press Officer Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA Phone: (405) 272-7159; E-mail: Adam-cohen@omrf.ouhsc.edu<
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Contact: Karen Honey
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
21-Sep-2006


Page: 1 2 3 4 5 6 7

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