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10.1038/s41598-018-28961-2 http://scihub22266oqcxt.onion/10.1038/s41598-018-28961-2 C6053440!6053440 !30026593     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30026593 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cellular stress induces erythrocyte assembly on intravascular von Willebrand factor strings and promotes microangiopathy |pdf=|usr=}}{{30026593 }} gab.com Text Cellular stress induces erythrocyte assembly on intravascular von Willebrand factor strings and promotes microangiopathy JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=30026593 #FOAvip Microangiopathy with subsequent organ damage represents a major complication in several diseases. The mechanisms leading to microvascular occlusion include von Willebrand factor (VWF), notably the formation of ultra-large von Willebrand factor fibers (ULVWFs) and platelet aggregation. To date, the contribution of erythrocytes to vascular occlusion is incompletely clarified. We investigated the platelet-independent interaction between stressed erythrocytes and ULVWFs and its consequences for microcirculation and organ function under dynamic conditions. In response to shear stress, erythrocytes interacted strongly with VWF to initiate the formation of ULVWF/erythrocyte aggregates via the binding of Annexin V to the VWF A1 domain. VWF-erythrocyte adhesion was attenuated by heparin and the VWF-specific protease ADAMTS13. In an in vivo model of renal ischemia/reperfusion injury, erythrocytes adhered to capillaries of wild-type but not VWF-deficient mice and later resulted in less renal damage. In vivo imaging in mice confirmed the adhesion of stressed erythrocytes to the vessel wall. Moreover, enhanced eryptosis rates and increased VWF binding were detected in blood samples from patients with chronic renal failure. Our study demonstrates that stressed erythrocytes have a pronounced binding affinity to ULVWFs. The discovered mechanisms suggest that erythrocytes are essential for the pathogenesis of microangiopathies and renal damage by actively binding to ULVWFs. Twit Text FOAVip Cellular stress induces erythrocyte assembly on intravascular von Willebrand factor strings and promotes microangiopathy ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=30026593 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30026593 #FOAvip English Wikipedia <ref>{{Cite pmid|30026593 }}</ref> Cellular stress induces erythrocyte assembly on intravascular von Willebrand factor strings and promotes microangiopathy #MMPMID30026593 Nicolay JP ; Thorn V ; Daniel C ; Amann K ; Siraskar B ; Lang F ; Hillgruber C ; Goerge T ; Hoffmann S ; Gorzelanny C ; Huck V ; Mess C ; Obser T ; Schneppenheim R ; Fleming I ; Schneider MF ; Schneider SW Sci Rep 2018[Jul]; 8 (1 ): 10945 PMID30026593 show ga Microangiopathy with subsequent organ damage represents a major complication in several diseases. The mechanisms leading to microvascular occlusion include von Willebrand factor (VWF), notably the formation of ultra-large von Willebrand factor fibers (ULVWFs) and platelet aggregation. To date, the contribution of erythrocytes to vascular occlusion is incompletely clarified. We investigated the platelet-independent interaction between stressed erythrocytes and ULVWFs and its consequences for microcirculation and organ function under dynamic conditions. In response to shear stress, erythrocytes interacted strongly with VWF to initiate the formation of ULVWF/erythrocyte aggregates via the binding of Annexin V to the VWF A1 domain. VWF-erythrocyte adhesion was attenuated by heparin and the VWF-specific protease ADAMTS13. In an in vivo model of renal ischemia/reperfusion injury, erythrocytes adhered to capillaries of wild-type but not VWF-deficient mice and later resulted in less renal damage. In vivo imaging in mice confirmed the adhesion of stressed erythrocytes to the vessel wall. Moreover, enhanced eryptosis rates and increased VWF binding were detected in blood samples from patients with chronic renal failure. Our study demonstrates that stressed erythrocytes have a pronounced binding affinity to ULVWFs. The discovered mechanisms suggest that erythrocytes are essential for the pathogenesis of microangiopathies and renal damage by actively binding to ULVWFs. |ADAMTS13 Protein/metabolism [MESH] |Animals [MESH] |Cell Adhesion [MESH] |Disease Models, Animal [MESH] |Erythrocytes/*cytology/metabolism [MESH] |Humans [MESH] |Mice [MESH] |Protein Domains [MESH] |Renal Insufficiency, Chronic/*metabolism [MESH] |Shear Strength [MESH] |Stress, Mechanical [MESH] |Vascular Diseases/*metabolism [MESH]Cellular stress induces erythrocyte assembly on intravascular von Will(epmc).pdf DeepDyve Pubget Overpricing