Annexin A8 controls leukocyte recruitment to activated endothelial cells via cell surface delivery of CD63

Michaela Poeter, Ines Brandherm, Jan Rossaint, Gonzalo Rosso, Victor Shahin, Boris V. Skryabin, Alexander Zarbock, Volker Gerke and Ursula Rescher ()
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Michaela Poeter: Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, and Interdisciplinary Clinical Research Center, University of Münster
Ines Brandherm: Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, and Interdisciplinary Clinical Research Center, University of Münster
Jan Rossaint: Intensive Care and Pain Medicine, University Hospital Münster
Gonzalo Rosso: Institute of Physiology II, University of Münster
Victor Shahin: Institute of Physiology II, University of Münster
Boris V. Skryabin: Institute of Experimental Pathology, Center for Molecular Biology of Inflammation, and Interdisciplinary Clinical Research Center, University of Münster
Alexander Zarbock: Intensive Care and Pain Medicine, University Hospital Münster
Volker Gerke: Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, and Interdisciplinary Clinical Research Center, University of Münster
Ursula Rescher: Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, and Interdisciplinary Clinical Research Center, University of Münster

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract To enable leukocyte adhesion to activated endothelium, the leukocyte receptor P-selectin is released from Weibel-Palade bodies (WPB) to the endothelial cell surface where it is stabilized by CD63. Here we report that loss of annexin A8 (anxA8) in human umbilical vein endothelial cells (HUVEC) strongly decreases cell surface presentation of CD63 and P-selectin, with a concomitant reduction in leukocyte rolling and adhesion. We confirm the compromised leukocyte adhesiveness in inflammatory-activated endothelial venules of anxA8-deficient mice. We find that WPB of anxA8-deficient HUVEC contain less CD63, and that this is caused by improper transport of CD63 from late multivesicular endosomes to WPB, with CD63 being retained in intraluminal vesicles. Consequently, reduced CD63 cell surface levels are seen following WPB exocytosis, resulting in enhanced P-selectin re-internalization. Our data support a model in which anxA8 affects leukocyte recruitment to activated endothelial cells by supplying WPB with sufficient amounts of the P-selectin regulator CD63.

Date: 2014
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DOI: 10.1038/ncomms4738

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