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The Clot Thickens: Protein Interaction Is A Drug Target For Blood Clot Prevention

Date:
July 16, 2007
Source:
Journal of Clinical Investigation
Summary:
After a blood vessel in injured, platelets cluster together to plug the site of injury in the form of a blood clot (thrombus). In arterial disease, altered platelet aggregation can block blood vessels and cause heart attack or stroke. Platelet aggregation involves the binding of many molecules to platelet integrin alpha-IIb beta 3, and blockade of this binding is effective in the prevention of blood clots. However, chronic use of oral drugs that block alpha-IIb beta 3 activation have not proved beneficial in preventing recurrent blood clots.
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After a blood vessel in injured, platelets cluster together to plug the site of injury in the form of a blood clot (thrombus). In arterial disease, altered platelet aggregation can block blood vessels and cause heart attack or stroke. Platelet aggregation involves the binding of many molecules to platelet integrin alpha-IIb beta 3, and blockade of this binding is effective in the prevention of blood clots. However, chronic use of oral drugs that block alpha-IIb beta 3 activation have not proved beneficial in preventing recurrent blood clots.

In a study appearing online on July 12 in advance of publication in the August print issue of the Journal of Clinical Investigation, Mark Ginsberg and colleagues from the University of California San Diego show that the binding of the protein talin to alpha-IIb beta 3 is critical for integrin activation in mice, and that selective disruption of the talin--alpha-IIb beta 3 interaction protects mice from pulmonary thromboembolism -- the formation of blood clots in the vessel that carries blood from the heart to the lungs.

Furthermore, this blockade results in very little pathological bleeding, which can often occur when the clotting process is disrupted.

The results suggest that modulation of the interaction between talin and alpha-IIb beta 3 could be an attractive strategy for the development of future anti-thrombotic drugs, with a reduced risk of pathological bleeding.


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The above post is reprinted from materials provided by Journal of Clinical Investigation. Note: Materials may be edited for content and length.


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Journal of Clinical Investigation. "The Clot Thickens: Protein Interaction Is A Drug Target For Blood Clot Prevention." ScienceDaily. ScienceDaily, 16 July 2007. <www.sciencedaily.com/releases/2007/07/070713233648.htm>.
Journal of Clinical Investigation. (2007, July 16). The Clot Thickens: Protein Interaction Is A Drug Target For Blood Clot Prevention. ScienceDaily. Retrieved July 29, 2015 from www.sciencedaily.com/releases/2007/07/070713233648.htm
Journal of Clinical Investigation. "The Clot Thickens: Protein Interaction Is A Drug Target For Blood Clot Prevention." ScienceDaily. www.sciencedaily.com/releases/2007/07/070713233648.htm (accessed July 29, 2015).

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