A key protein controlling the stickiness of blood has been identified, which could lead to the development of new drugs to reduce the risk of heart attacks and strokes.
Small cells called platelets circulate in the blood and respond to injury by becoming sticky and sending out tiny 鈥渁rms鈥� that latch onto other platelets and the surface of the injury, forming a clot.
But platelets aren鈥檛 sticky all the time. , a British Heart Foundation researcher at the University of Birmingham, UK, and his colleagues had previously identified a protein called CD148.
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Clot reduction
The team suspected the protein might be involved in initiating the clotting process in response to tissue injury, since it belongs to a class of proteins that control the activity of other proteins.
To investigate further, they compared platelets from mice engineered to lack CD148, with those from normal mice. Platelets from mice lacking the protein were more sluggish in responding to injury, sent out fewer arms and formed smaller clots.
Importantly for the safety of any future blood-thinning medicine, removing CD148 didn鈥檛 cause any dangerous bleeding. This may be because several other pathways can also trigger clotting.
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Existing blood-thinners like aspirin irreversibly block all of these pathways until the body removes the platelet from the circulation (after about 7 to 10 days). This means that they can trigger dangerous bleeding in some patients, particularly in the stomach. 鈥淭hey鈥檙e a blunt instrument,鈥� says Senis.
A drug that reversibly blocked CD148 would be safer because it would only affect one pathway, dampening clotting but leaving some control over bleeding.
Alternatively, drugs could be developed that enhance platelet stickiness to reduce bleeding in some situations. 鈥淧erhaps soldiers could carry a little kit around with them,鈥� Senis says.
鈥淐D148 looks very promising as a realistic target for new drug development,鈥� adds Jeremy Pearson, Associate Medical Director at the British Heart Foundation.
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