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Updated: Aug 11, 2026

A Novel In vitro Model for Studying the Interactions Between Human Whole Blood and Endothelium
Published on: November 21, 2014
Lack of in vivo function of CD31 in vascular thrombosis
1Institute for Clinical and Experimental Surgery, University of Saarland, Homburg/Saar, Germany. exbvol@med-rz.uni-sb.de
A murine model of endothelial cell injury-based vascular thrombosis was used to test the role of platelet-endothelial cell adhesion molecule-1 (PECAM-1, CD31) in blood cell aggregate formation and vessel occlusion in vivo. Photochemically-induced thrombus formation was analyzed in detail using intravital fluorescence microscopy of individual microvessels in cremaster muscle preparations of CD31-deficient and wildtype mice. In venules, epi-illumination induced rapid thrombus formation with first platelet deposition after 0.56 +/- 0.11 min and complete vessel occlusion within 5.05 +/- 0.45 min. In arterioles, thrombus formation was markedly delayed with first platelet deposition after 3.03 +/- 0.47 min and complete vessel occlusion within 10.04 +/- 1.26 min. Kinetics of thrombus formation in both venules (first platelet deposition: 0.52 +/- 0.1 min; vessel occlusion: 5.03 +/- 0.52 min) and arterioles (first platelet deposition: 3.06 +/- 0.68 min; vessel occlusion: 10.02 +/- 1.38 min) of CD31-deficient mice was found almost identical compared with that in wildtype animals. Tail bleeding time was 233 +/- 24 s in wildtype and 243 +/- 32 s in CD31-deficient mice. Moreover, CD31-deficient and wildtype mice revealed comparable interaction of leukocytes to endothelium. This study shows for the first time in vivo that CD31 is not critically involved in blood cell thrombus formation upon endothelial cell injury.
A murine model of endothelial cell injury-based vascular thrombosis was used to test the role of platelet-endothelial cell adhesion molecule-1 (PECAM-1, CD31) in blood cell aggregate formation and vessel occlusion in vivo. Photochemically-induced thrombus formation was analyzed in detail using intravital fluorescence microscopy of individual microvessels in cremaster muscle preparations of CD31-deficient and wildtype mice. In venules, epi-illumination induced rapid thrombus formation with first platelet deposition after 0.56 +/- 0.11 min and complete vessel occlusion within 5.05 +/- 0.45 min. In arterioles, thrombus formation was markedly delayed with first platelet deposition after 3.03 +/- 0.47 min and complete vessel occlusion within 10.04 +/- 1.26 min. Kinetics of thrombus formation in both venules (first platelet deposition: 0.52 +/- 0.1 min; vessel occlusion: 5.03 +/- 0.52 min) and arterioles (first platelet deposition: 3.06 +/- 0.68 min; vessel occlusion: 10.02 +/- 1.38 min) of CD31-deficient mice was found almost identical compared with that in wildtype animals. Tail bleeding time was 233 +/- 24 s in wildtype and 243 +/- 32 s in CD31-deficient mice. Moreover, CD31-deficient and wildtype mice revealed comparable interaction of leukocytes to endothelium. This study shows for the first time in vivo that CD31 is not critically involved in blood cell thrombus formation upon endothelial cell injury.
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