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Prepublished online as a Blood First Edition Paper on June 26, 2003; DOI 10.1182/blood-2003-01-0080. This Article Full Text (PDF) All Versions of this Article: 2003-01-0080v1 102/8/2828    most recent Alert me when this article is cited Alert me if a correction is posted 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 Sheikh, S. Articles by Nash, G. B Search for Related Content PubMed PubMed Citation Articles by Sheikh, S. Articles by Nash, G. B Social Bookmarking                   What's this? Submitted January 10, 2003 Accepted June 19, 2003 Exposure to fluid shear stress modulates the ability of endothelial cells to recruit neutrophils in response to tumour necrosis factor-: a basis for local variations in vascular sensitivity to inflammation Sajila Sheikh, George Ed Rainger, Zoe Gale, Mahbub Rahman, and Gerard B Nash* Department of Physiology, The Medical School, University of Birmingham, Birmingham, United Kingdom * Corresponding author; email: g.nash{at}bham.ac.uk. Vascular endothelial cells are able to sense changes in the forces acting on them and respond, for instance, by modifying expression of a range of genes. However, there is little information on how such responses are integrated to modify homeostatic functions. We hypothesised that different shear stresses experienced in different regions of the circulation might influence endothelial sensitivity to inflammatory stimuli. We cultured human endothelial cells in tubes, and exposed them for varying periods to shear stresses ranging from those typically found in post-capillary venules to those in arteries. When tumour necrosis factor- was included in the flow cultures, we found startling differential effects of shear stress on the ability of endothelial cells to induce adhesion and migration of flowing neutrophils. Compared to static cultures, endothelial cells cultured at low shear stress (0.3Pa) captured similar numbers of neutrophils, but failed to induce their transendothelial migration. After exposure of endothelial cells to high shear stress (1.0 or 2.0Pa), capture of neutrophils was largely ablated. The modification in response was detectable after 4 hours of exposure to flow, but was much greater after 24 hours. From analysis of gene expression, loss of capture or migration was attributable to reduction in tumour necrosis factor-induced expression of selectins or CXC-chemokines respectively. Thus, conditioning of endothelial cells by different flow environments may underly variations in susceptibility to inflammation between different tissues or parts of the vascular tree. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Duchene, C. Cayla, S. Vessillier, R. Scotland, K. Yamashiro, F. Lecomte, I. Syed, P. Vo, A. Marrelli, C. Pitzalis, et al. Laminar Shear Stress Regulates Endothelial Kinin B1 Receptor Expression and Function: Potential Implication in Atherogenesis Arterioscler Thromb Vasc Biol, November 1, 2009; 29(11): 1757 - 1763. [Abstract] [Full Text] [PDF] M. Zakkar, K. Van der Heiden, L. A. Luong, H. Chaudhury, S. Cuhlmann, S. S. Hamdulay, R. Krams, I. Edirisinghe, I. Rahman, H. Carlsen, et al. Activation of Nrf2 in Endothelial Cells Protects Arteries From Exhibiting a Proinflammatory State Arterioscler Thromb Vasc Biol, November 1, 2009; 29(11): 1851 - 1857. 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