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Blood, 1 May 2007, Vol. 109, No. 9, pp. 3741-3744. Prepublished online as a Blood First Edition Paper on January 9, 2007; DOI 10.1182/blood-2006-05-022566. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2006-05-022566v1 109/9/3741    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Moraes, L. A. Articles by Bishop-Bailey, D. Search for Related Content PubMed PubMed Citation Articles by Moraes, L. A. Articles by Bishop-Bailey, D. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Nongenomic signaling of the retinoid X receptor through binding and inhibiting Gq in human platelets Leonardo A. Moraes1, Karen E. Swales1, Jessica A. Wray1, Amilcar Damazo2, Jonathan M. Gibbins3, Timothy D. Warner1, and David Bishop-Bailey1 1 Cardiac, Vascular and Inflammation Research 2 Biochemical Pharmacology, William Harvey Research Institute, Barts and the London, Queen Mary University of London, United Kingdom; and 3 School of Biological Sciences, The University of Reading, United Kingdom Retinoid X receptors (RXRs) are important transcriptional nuclear hormone receptors, acting as either homodimers or the binding partner for at least one fourth of all the known human nuclear receptors. Functional nongenomic effects of nuclear receptors are poorly understood; however, recently peroxisome proliferator-activated receptor (PPAR) \#947;, PPAR\#946;, and the glucocorticoid receptor have all been found active in human platelets. Human platelets express RXR\#945; and RXR\#946;. RXR ligands inhibit platelet aggregation and TXA2 release to ADP and the TXA2 receptors, but only weakly to collagen. ADP and TXA2 both signal via the G protein, Gq. RXR rapidly binds Gq but not Gi/z/o/t/gust in a ligand-dependent manner and inhibits Gq-induced Rac activation and intracellular calcium release. We propose that RXR ligands may have beneficial clinical actions through inhibition of platelet activation. Furthermore, our results demonstrate a novel nongenomic mode for nuclear receptor action and a functional cross-talk between G-protein and nuclear receptor signaling families. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y.-H. Han, H. Zhou, J.-H. Kim, T.-d. Yan, K.-H. Lee, H. Wu, F. Lin, N. Lu, J. Liu, J.-z. Zeng, et al. A Unique Cytoplasmic Localization of Retinoic Acid Receptor-{gamma} and Its Regulations J. Biol. Chem., July 3, 2009; 284(27): 18503 - 18514. [Abstract] [Full Text] [PDF] X. Ruan, F. Zheng, and Y. Guan PPARs and the kidney in metabolic syndrome Am J Physiol Renal Physiol, May 1, 2008; 294(5): F1032 - F1047. [Abstract] [Full Text] [PDF] J. A. Mitchell, F. Ali, L. Bailey, L. Moreno, and L. S. Harrington Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium Exp Physiol, January 1, 2008; 93(1): 141 - 147. [Abstract] [Full Text] [PDF]

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