The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
von Willebrand factor–cleaving protease ADAMTS13 reduces ischemic brain injury in experimental stroke
Open accessAbstract
Stroke is a leading cause of death and disability. The only therapy available is recombinant tissue plasminogen activator, but side effects limit its use. Platelets play a crucial role during stroke, and the inflammatory reaction promotes neurodegeneration. von Willebrand factor (VWF), an adhesion molecule for platelets, is elevated in patients with acute stroke. The activity of VWF is modulated by ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type I repeats-13) that cleaves VWF to smaller less-active forms. We recently documented that ADAMTS13 negatively regulates both thrombosis and inflammation. We report that deficiency or reduction of VWF reduces infarct volume up to 2-fold after focal cerebral ischemia in mice, thus showing the importance of VWF in stroke injury. In contrast, ADAMTS13 deficiency results in larger infarctions, but only in mice that have VWF. Importantly, infusion of a high dose of recombinant human ADAMTS13 into a wild-type mouse immediately before reperfusion reduces infarct volume and improves functional outcome without producing cerebral hemorrhage. Furthermore, recombinant ADAMTS13 did not enhance bleeding in a hemorrhagic stroke model. Our findings show the importance of VWF in regulating infarction and suggest that recombinant ADAMTS13 could be considered as a new therapeutic agent for prevention and/or treatment of stroke.
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Self-citationFRETS‐VWF73, a first fluorogenic substrate for ADAMTS13 assay
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Self-citationVon Willebrand factor, ADAMTS13, and thrombotic thrombocytopenic purpura
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Experimental Stroke Induces Massive, Rapid Activation of the Peripheral Immune System
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A mouse model of severe von Willebrand disease: Defects in hemostasis and thrombosis
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Self-citation
Cited by
Thrombosis: tangled up in NETs
Martinod, K., & Wagner, D. D. (2014) · Blood · doi:10.1182/blood-2013-10-463646 · Cited by 866
Self-citationKalogeris, T., Baines, C. P., Krenz, M., & Korthuis, R. J. (2016) · Comprehensive Physiology · doi:10.1002/cphy.c160006 · Cited by 718
von Willebrand factor, Jedi knight of the bloodstream
Springer, T. A. (2014) · Blood · doi:10.1182/blood-2014-05-378638 · Cited by 444
Platelet adhesion and activation mechanisms in arterial thrombosis and ischaemic stroke
NIESWANDT, B., PLEINES, I., & BENDER, M. (2011) · Journal of Thrombosis and Haemostasis · doi:10.1111/j.1538-7836.2011.04361.x · Cited by 356
Ischaemic stroke: a thrombo‐inflammatory disease?
Nieswandt, B., Kleinschnitz, C., & Stoll, G. (2011) · The Journal of Physiology · doi:10.1113/jphysiol.2011.212886 · Cited by 192
Metadata
- Authors
- Zhao, B.-Q., Chauhan, A. K., Canault, M., Patten, I. S., Yang, J. J., Dockal, M., Scheiflinger, F., & Wagner, D. D.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2009-10-08
- Volume
- 114
- Issue
- 15
- Pages
- 3329-3334
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2049710061
- Cited by
- 269
- References
- 29
- FWCI
- 10.30
- Type
- journal article
- Language
- en
- Open access
- green
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- Zhao, B.-Q., Chauhan, A. K., Canault, M., Patten, I. S., Yang, J. J., Dockal, M., Scheiflinger, F., & Wagner, D. D. (2009). von Willebrand factor–cleaving protease ADAMTS13 reduces ischemic brain injury in experimental stroke. Blood. https://doi.org/10.1182/blood-2009-03-213264
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