Journal
OLIGONUCLEOTIDES
Volume 17, Issue 3, Pages 265-274Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/oli.2007.0089
Keywords
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL065222] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL65222] Funding Source: Medline
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Thrombus formation is initiated by platelets and leads to cardiovascular, cerebrovascular, and peripheral vascular disease, the leading causes of morbidity and mortality in the Western world. A number of antiplatelet drugs have improved clinical outcomes for thrombosis patients. However, their expanded use, especially in surgery, is limited by hemorrhage. Here, we describe an antiplatelet agent that can have its activity controlled by a matched antidote. We demonstrate that an RNA aptamer targeting von Willebrand factor ( VWF) can potently inhibit VWF- mediated platelet adhesion and aggregation. By targeting this important adhesion step, we show that the aptamer molecule can inhibit platelet aggregation in PFA- 100 and ristocetin- induced platelet aggregation assays. Furthermore, we show that a rationally designed antidote molecule can reverse the effects of the aptamer molecule, restoring platelet function quickly and effectively over a clinically relevant period. This aptamerantidote pair represents a reversible antiplatelet agent inhibiting a platelet specific pathway. Furthermore, it is an important step towards creating safer drugs in clinics through the utilization of an antidote molecule.
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