A dual role for integrin-linked kinase in platelets: Regulating integrin function and {alpha}-granule secretion

Katherine L. Tucker, Tanya Sage, Joanne M. Stevens, Peter A. Jordan, Sarah Jones, Natasha E. Barrett, Rene St-Arnaud, Jonathan Frampton, Shoukat Dedhar, Jonathan M. Gibbins

    Research output: Contribution to journalArticlepeer-review


    Integrin-linked kinase (ILK) has been implicated in the regulation of a range of fundamental biological processes such as cell survival, growth, differentiation, and adhesion. In platelets ILK associates with β1- and β3-containing integrins, which are of paramount importance for the function of platelets. Upon stimulation of platelets this association with the integrins is increased and ILK kinase activity is up-regulated, suggesting that ILK may be important for the coordination of platelet responses. In this study a conditional knockout mouse model was developed to examine the role of ILK in platelets. The ILK-deficient mice showed an increased bleeding time and volume, and despite normal ultrastructure the function of ILK-deficient platelets was decreased significantly. This included reduced aggregation, fibrinogen binding, and thrombus formation under arterial flow conditions. Furthermore, although early collagen stimulated signaling such as PLCγ2 phosphorylation and calcium mobilization were unaffected in ILK-deficient platelets, a selective defect in α-granule, but not dense-granule, secretion was observed. These results indicate that as well as involvement in the control of integrin affinity, ILK is required for (v-granule secretion and therefore may play a central role in the regulation of platelet function. © 2008 by The American Society of Hematology.
    Original languageEnglish
    Pages (from-to)4523-4531
    Number of pages8
    Issue number12
    Publication statusPublished - 1 Dec 2008


    • Animals
    • Blood Platelets/*enzymology/metabolism
    • Cloning, Molecular
    • Hemorrhage/genetics
    • Mice
    • Mice, Inbred C57BL
    • Mice, Knockout
    • Platelet Activation/*genetics
    • Platelet Aggregation/genetics
    • Platelet Glycoprotein GPIIb-IIIa Complex/physiology
    • Protein-Serine-Threonine Kinases/genetics/metabolism/*physiology
    • Secretory Vesicles/*secretion
    • Thrombosis/genetics


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