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Blood, 1 April 2007, Vol. 109, No. 7, pp. 2854-2862. Prepublished online as a Blood First Edition Paper on November 21, 2006; DOI 10.1182/blood-2006-06-026187. This Article Full Text Full Text (PDF) Supplemental Table and Figure All Versions of this Article: blood-2006-06-026187v1 109/7/2854    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 Kirsch, T. Articles by Haubitz, M. Search for Related Content PubMed PubMed Citation Articles by Kirsch, T. Articles by Haubitz, M. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Engulfment of apoptotic cells by microvascular endothelial cells induces proinflammatory responses Torsten Kirsch1, Alexander Woywodt1, Michaela Beese1, Kristin Wyss1, Joon-Keun Park1, Uta Erdbruegger1, Barbara Hertel1, Hermann Haller1, and Marion Haubitz1 1 Division of Nephrology, Department of Medicine, Hannover Medical School, Hannover, Germany Circulating endothelial cells (CECs) have been detected in a variety of vascular disorders, but their interactions with healthy endothelium remain unknown. The aim of this study was to evaluate the response of human endothelial cells (ECs) to apoptotic or necrotic ECs in an in vitro model and to delineate pathogenetic pathways. Here we show that incubation of the human microvascular endothelial cell line (HMEC-1) with apoptotic ECs resulted in increased expression of chemokines and enhanced binding of leukocytes to HMEC-1 cells, whereas exposure of HMEC-1 cells to necrotic ECs caused no changes in leukocyte-binding affinity. Both apoptotic and necrotic cells were bound and engulfed by HMEC-1 cells and primary human umbilical vein endothelial cells (HUVECs). We therefore suggest that exposures to apoptotic and necrotic ECs induce different patterns of chemokine synthesis and leukocyte adhesion in healthy ECs. These data indicate that CECs are not only markers of vascular damage but may induce proinflammatory signals in the endothelium. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. A. O'Brien, M. A. Richardson, D. T. Berg, B. Gerlitz, A. Gupta, and B. W. Grinnell The Puzzling Role of TRAIL in Endothelial Cell Biology Arterioscler. Thromb. Vasc. Biol., February 1, 2008; 28(2): e5 - e6. [Full Text] [PDF] A. Woywodt, T. Kirsch, and M. Haubitz Circulating endothelial cells in renal disease: markers and mediators of vascular damage Nephrol. Dial. Transplant., January 1, 2008; 23(1): 7 - 10. [Full Text] [PDF]

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