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Blood, 15 December 2008, Vol. 112, No. 13, pp. 4935-4939. Prepublished online as a Blood First Edition Paper on September 16, 2008; DOI 10.1182/blood-2008-04-151043. This Article Full Text Full Text (PDF) Supplemental Figures Erratum (v114,p1281) All Versions of this Article: blood-2008-04-151043v1 112/13/4935    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 Verhaar, R. Articles by Verhoeven, A. J. Search for Related Content PubMed PubMed Citation Articles by Verhaar, R. Articles by Verhoeven, A. J. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY UV-C irradiation disrupts platelet surface disulfide bonds and activates the platelet integrin IIbβ3 Robin Verhaar1, David W. C. Dekkers1, Iris M. De Cuyper1, Mark H. Ginsberg2, Dirk de Korte1, and Arthur J. Verhoeven1 1 Department of Blood Cell Research, Sanquin Research, Amsterdam, The Netherlands; and 2 Department of Medicine, University of California San Diego, La Jolla UV-C irradiation has been shown to be effective for pathogen reduction in platelet concentrates, but preliminary work indicated that UV-C irradiation of platelets can induce platelet aggregation. In this study, the mechanism underlying this phenomenon was investigated. Irradiation of platelets with UV-C light (1500 J/m2) caused platelet aggregation, which was dependent on integrin IIbβ3 activation (GPIIb/IIIa). This activation occurred despite treatment with several signal transduction inhibitors known to block platelet activation. UV-C also induced activation of recombinant IIbβ3 in Chinese hamster ovary (CHO) cells, an environment in which physiologic agonists fail to activate. Activation of IIbβ3 requires talin binding to the β3 tail, yet IIbβ3-724 (lacking the talin binding site) was activated by UV-C irradiation, excluding a requirement for talin binding. The UV-C effect appears to be general in that β1 and β2 integrins are also activated by UV-C. To explain these findings, we investigated the possibility of UV-C–induced photolysis of disulfide bonds, in analogy with the activating effect of reducing agents on integrins. Indeed, UV-C induced a marked increase in free thiol groups in platelet surface proteins including IIbβ3. Thus, UV-C appears to activate IIbβ3 not by affecting intracellular signal transduction, but by reduction of disulfide bonds regulating integrin conformation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: UV-C irradiation gives platelets a sunburn Joel S. Bennett Blood 2008 112: 4784-4785. [Full Text] [PDF] This article has been cited by other articles: T. W. Kuijpers, E. van de Vijver, M. A. J. Weterman, M. de Boer, A. T. J. Tool, T. K. van den Berg, M. Moser, M. E. Jakobs, K. Seeger, O. Sanal, et al. LAD-1/variant syndrome is caused by mutations in FERMT3 Blood, May 7, 2009; 113(19): 4740 - 4746. [Abstract] [Full Text] [PDF]

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