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Blood, 15 January 2007, Vol. 109, No. 2, pp. 616-618. Prepublished online as a Blood First Edition Paper on September 21, 2006; DOI 10.1182/blood-2006-07-038158. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-07-038158v1 109/2/616    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 Begonja, A. J. Articles by Walter, U. Search for Related Content PubMed PubMed Citation Articles by Begonja, A. J. Articles by Walter, U. Related Collections Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Brief report Thrombin stimulation of p38 MAP kinase in human platelets is mediated by ADP and thromboxane A2 and inhibited by cGMP/cGMP-dependent protein kinase Antonija Jurak Begonja1, Jörg Geiger1, Natalia Rukoyatkina1,2, Steffen Rauchfuss1, Stepan Gambaryan1,2,, and Ulrich Walter1, 1 Institute of Clinical Biochemistry and Pathobiochemistry, University of Würzburg, Germany; 2 Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St Petersburg, Russia p38 MAP kinase in human platelets is activated by platelet agonists including thrombin, thromboxane A2 (TxA2), ADP, and others. However, both upstream mechanisms of p38 MAP kinase activation, and their downstream sequelae, are presently controversial and essentially unclear. Certain studies report sequential activation of cGMP-dependent protein kinase (PKG) and p38/ERK pathways by platelet agonists, leading to integrin activation and secretion, whereas others establish an essential role of Src/ERK-mediated TxA2 generation for fibrinogen receptor activation in human platelets. Here, we show that ADP secreted from platelet-dense granules, and subsequent activation of P2Y12 receptors, as well as TxA2 release are important upstream mediators of p38 MAP kinase activation by thrombin. However, p38 MAP kinase activation did not significantly contribute to calcium mobilization, P-selectin expression, IIbß3 integrin activation, and aggregation of human platelets in response to thrombin. Finally, PKG activation did not stimulate, but rather inhibited, p38 MAP kinase in human platelets. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Sun, A. Swaim, J. E. Herrera, D. Becker, L. Becker, K. Srivastava, L. E. Thompson, M. R. Shero, A. Perez-Tamayo, B. Suktitipat, et al. Platelet Kainate Receptor Signaling Promotes Thrombosis by Stimulating Cyclooxygenase Activation Circ. Res., September 11, 2009; 105(6): 595 - 603. [Abstract] [Full Text] [PDF] M. Jing, V. K Cheruvu, and F. Ismail-Beigi Stimulation of glucose transport in response to activation of distinct AMPK signaling pathways Am J Physiol Cell Physiol, November 1, 2008; 295(5): C1071 - C1082. [Abstract] [Full Text] [PDF]

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