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Blood, 15 October 2003, Vol. 102, No. 8, pp. 2828-2834. Prepublished online as a Blood First Edition Paper on June 26, 2003; DOI 10.1182/blood-2003-01-0080. This Article Full Text 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 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 Sheikh, S. Articles by Nash, G. B. Search for Related Content PubMed PubMed Citation Articles by Sheikh, S. Articles by Nash, G. B. Related Collections Hemostasis, Thrombosis, and Vascular Biology Phagocytes Cell Adhesion and Motility Signal Transduction Gene Expression Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Exposure to fluid shear stress modulates the ability of endothelial cells to recruit neutrophils in response to tumor necrosis factor-: a basis for local variations in vascular sensitivity to inflammation Sajila Sheikh, G. Ed Rainger, Zoe Gale, Mahbub Rahman, and Gerard B. Nash From the Department of Physiology, Division of Medical Sciences, The Medical School, The University of Birmingham, Birmingham, United Kingdom. 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 hypothesized 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 postcapillary venules to those in arteries. When tumor 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 with static cultures, endothelial cells cultured at low shear stress (0.3 Pa) captured similar numbers of neutrophils but failed to induce their transendothelial migration. After exposure of endothelial cells to high shear stress (1.0 or 2.0 Pa), 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 tumor necrosis factor–induced expression of selectins or CXC-chemokines, respectively. Thus, conditioning of endothelial cells by different flow environments may underlie 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. [Abstract] [Full Text] [PDF] Q. Zhao, X. Guo, G. B. Nash, P. C. Stone, J. Hilkens, J. M. Rhodes, and L.-G. Yu Circulating Galectin-3 Promotes Metastasis by Modifying MUC1 Localization on Cancer Cell Surface Cancer Res., September 1, 2009; 69(17): 6799 - 6806. [Abstract] [Full Text] [PDF] S. S. Shaik, T. D. Soltau, G. Chaturvedi, B. Totapally, J. S. Hagood, W. W. Andrews, M. Athar, N. N. Voitenok, C. R. Killingsworth, R. P. Patel, et al. Low Intensity Shear Stress Increases Endothelial ELR+ CXC Chemokine Production via a Focal Adhesion Kinase-p38{beta} MAPK-NF-{kappa}B Pathway J. Biol. Chem., February 27, 2009; 284(9): 5945 - 5955. [Abstract] [Full Text] [PDF] A. R. Kinderlerer, F. Ali, M. Johns, E. A. 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Bautch Orientation of endothelial cell division is regulated by VEGF signaling during blood vessel formation Blood, February 15, 2007; 109(4): 1345 - 1352. [Abstract] [Full Text] [PDF] J. W. Calderwood, J. M. Williams, M. D. Morgan, G. B. Nash, and C. O. S. Savage ANCA induces {beta}2 integrin and CXC chemokine-dependent neutrophil-endothelial cell interactions that mimic those of highly cytokine-activated endothelium J. Leukoc. Biol., January 1, 2005; 77(1): 33 - 43. [Abstract] [Full Text] [PDF]

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