Interaction of Platelet Proteins Controls Clotting

Researchers have identified a protein that acts as an endogenous anticoagulant and prevents the activation of the platelet proteins that cause blood to clot.

Investigators at the University of North Carolina (Chapel Hill, USA) focused their attention on the calcium and integrin binding protein CIB1. This is a platelet integral membrane protein that binds to another protein called GPIIb/IIIa. GPIIb/IIIa is normally present in the membrane in an inactive, resting conformation. However, in the current study, published in the January 17, 2006, issue of the Journal of Cell Biology, the authors reported that reduction of CIB1 by RNA interference (RNAi) gene silencing caused activation of GPIIb/IIIa. Likewise, cells where GPIIb/IIIa were overexpressed tended to clot.

"Our data suggest that CIB1 may be one of the body's own natural anti-coagulants--as long as CIB1 is bound to GPIIb/IIIa, the platelet stays quiet. However, if a person does not have enough CIB1 or their CIB1 is not functional, then their platelets may have the potential to be hyper-responsive and pathologically predisposed to clotting,” explained senior author Dr. Leslie V. Parise, professor of pharmacology at the University of North Carolina.



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