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. 2017 Jun 13;7:3413. doi: 10.1038/s41598-017-03597-w

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Effect of hemodynamic shear stress on transfusion-induced endothelial injury. (A,B) Endothelial perfusion with RBCs at a sub-physiological level of shear stress (0.14 dyn/cm²) gives rise to marked downregulation of nuclear HMGB1 expression (“low shear transfusion”), indicating severe necroptosis in the microvascular endothelium (***p < 0.001; n = 3). “Low shear control” refers to perfusion of the microfluidic endothelium at 0.14 dyn/cm² with culture medium alone. Blue shows nuclear staining. (C,D) Qualitative and quantitative comparisons of transfusion-induced nuclear HMGB1 loss between the sub-physiological “low shear” (0.14 dyn/cm²) and physiological “high shear” (14.8 dyn/cm²) conditions. RBC perfusion at physiological shear stress results in significantly smaller HMGB1 reduction, suggesting the protective role of physiological hemodynamic microenvironment. Scale bars: 50 μm.