Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 106, Issue 3, Pages 385-392Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI9896
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Funding
- NHLBI NIH HHS [R37 HL-41002, R37 HL041002, P01 HL-414484, R01 HL-47826] Funding Source: Medline
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We used intravital microscopy to observe the formation of platelet plugs in ferric chloride-injured arterioles of live mice. With this model, we evaluated thrombus growth in mice lacking von Willebrand factor (vWF) and fibrinogen (Fg), the two key ligands known to mediate platelet adhesion and aggregation. In vWF(-/-) mice, despite the presence of arterial shear, delayed platelet adhesion occurred and stable thrombi formed, In many mice, a persisting high-shear channel never occluded. Abundant thrombi formed in Fg(-/-) mice, but they detached from the subendothelium, which ultimately caused downstream occlusion in all cases. Surprisingly, mice deficient in both VWF and Fg successfully formed thrombi with properties characteristic of both mutations, leading to vessel occlusion in the majority of vessels, platelets of these doubly deficient mice specifically accumulated fibronectin in their alpha-granules, suggesting that fibronectin could be the ligand supporting the platelet aggregation.
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