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J. Lipid Res.
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A more recent version of this article appeared on June 1, 2009 Originally published In Press as doi:10.1194/jlr.M800447-JLR200 on April 7, 2009 Originally published In Press as doi:10.1194/jlr.M800447-JLR200 on April 3, 2009 Originally published In Press as doi:10.1194/jlr.M800447-JLR200 on January 16, 2009

Papers In Press, published online ahead of print April 2, 2009
J. Lipid Res., doi:10.1194/jlr.M800447-JLR200
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Submitted on August 21, 2008
Revised on December 29, 2008
Accepted on January 16, 2009

Activation dependent stabilization of the human thromboxane receptor: Role of reactive oxygen species

Stephen J Wilson, Claire C. Cavanaugh, Allison M Lesher, Alexander J Frey, Shane E Russell, and Emer M Smyth

Pharmacology, University of Pennsylvania, Philadelphia, PA 19104

Corresponding Author: emsmyth{at}mail.med.upenn.edu

Thromboxane A<SUB>2</SUB> (TxA<SUB>2</SUB>), the principle product of platelet COX-1 dependent arachidonic acid metabolism, directs multiple pro-atherogenic processes via its receptor, the TP. Oxidative challenge offset TP degradation, a key component in limiting TxA<SUB>2</SUB>&#146; actions. Following TP activation, we observed cellular reactive oxygen species (ROS) generation coincident with increased TP expression. We examined the link between TP-evoked ROS and TP regulation. TP expression was augmented in TP<IMG SRC="/math/alpha.gif" ALIGN="BASELINE" ALT="alpha "> transfected cells, treated with a TxA<SUB>2</SUB> analog (IBOP). This was reduced with a cellular antioxidant, N-acetyl cysteine, or two distinct NADPH oxidases inhibitors, diphenyleneiodonium (DPI) and apocynin. Homologous upregulation of the native TP was also reduced in apocynin-treated aortic smooth muscle cells (ASMC) and was absent in ASMC lacking an NADPH oxidase subunit (p47-/-). TP transcription was not increased in IBOP treated cells indicating a post-transcriptional mechanism. IBOP induced translocation of TP<IMG SRC="/math/alpha.gif" ALIGN="BASELINE" ALT="alpha "> to the Golgi and reduced degradation of the immature form of the receptor. These data are consistent with a ROS-dependent mechanism whereby TP activation enhanced TP stability, early in post-transcriptional biogenesis. Given the significant role played by TP and ROS in perturbed cardiovascular function, the convergence of TP on ROS-generating pathways for regulation of TxA<SUB>2</SUB>-dependent events may be critical for cardiovascular disease.


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