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Blood, 1 July 2004, Vol. 104, No. 1, pp. 100-106. Prepublished online as a Blood First Edition Paper on March 16, 2004; DOI 10.1182/blood-2004-01-0107. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-01-0107v1 104/1/100    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 Bernardo, A. Articles by Dong, J.-f. Search for Related Content PubMed PubMed Citation Articles by Bernardo, A. Articles by Dong, J.-f. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Cell Adhesion and Motility Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Effects of inflammatory cytokines on the release and cleavage of the endothelial cell–derived ultralarge von Willebrand factor multimers under flow Aubrey Bernardo, Chalmette Ball, Leticia Nolasco, Joel F. Moake, and Jing-fei Dong From the Thrombosis Research Section, Department of Medicine, Baylor College of Medicine, Houston, TX. ADAMTS13 cleaves ultralarge and hyperreactive von Willebrand factor (ULVWF) freshly released from activated endothelial cells to smaller and less active forms. This process may be affected by the amount of ULVWF released and the processing capacity of ADAMTS13, contributing to the development of thrombotic diseases. We examined the effects of inflammatory cytokines on the release and cleavage of ULVWF to evaluate potential links between inflammation and thrombosis. Human umbilical vein endothelial cells were treated with interleukin 6 (IL-6), IL-8, or tumor necrosis factor (TNF-), and the formation of platelet-decorated ULVWF strings was quantitated. IL-8 and TNF- significantly stimulated the release of ULVWF in a dose-dependent manner. IL-6 induced ULVWF release only when it was in complex with the soluble IL-6 receptor. IL-6, but not IL-8 nor TNF-, inhibited the cleavage of ULVWF strings by ADAMTS13 under flowing, but not static, conditions. These results suggest that inflammatory cytokines may stimulate the ULVWF release (IL-8 and TNF-) and inhibit the ULVWF cleavage (IL-6), resulting in the accumulation of hyperreactive ULVWF in plasma and on the surface of endothelial cells to induce platelet aggregation and adhesion on the vascular endothelium. The findings describe a potential linkage between inflammation and thrombosis that may be of therapeutic importance. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: ADAMTS-13, VWF, inflammation, and thrombosis David G. Motto Blood 2004 104: 4-5. [Full Text] [PDF] This article has been cited by other articles: J. A. Kellum and D. C. Angus Mortality in Humans With Pneumonia and Sepsis Is Related to an Uncompensated Anti-inflammatory Response to Infection--Reply Arch Intern Med, July 14, 2008; 168(13): 1469 - 1469. [Full Text] [PDF] H.-H. Wang, C.-I Kung, Y.-Y. Tseng, Y.-C. Lin, C.-H. Chen, C.-H. Tsai, and H.-I Yeh Activation of endothelial cells to pathological status by down-regulation of connexin43 Cardiovasc Res, May 17, 2008; (2008) cvn112v2. [Abstract] [Full Text] [PDF] M. Nosaka, Y. Ishida, A. Tanaka, T. Hayashi, T. Miyashita, C. Kaminaka, W. Eisenmenger, F. Furukawa, and A. 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