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KMID : 0578320110320040333
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Molecules and Cells
2011 Volume.32 No. 4 p.333 ~ p.336
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Wnt5a Potentiates U46619-Induced Platelet Aggregation via the PI3K/Akt Pathway
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Kim Sun-Young
Kim Se-Woon
YunChoi Hye-Sook
Jho Eek-Hoon
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Abstract
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Platelet aggregation plays crucial roles in the formation of hemostatic plugs and thrombosis. Although it was recen-tly shown that canonical Wnt signaling negatively regulates platelet aggregation, the role of non-canonical Wnt signaling remains unknown. Here, we observed that Wnt5a, one of the non-canonical Wnts, positively regulated platelet aggregation. Platelet aggregation was potentiated by the addition of Wnt5a to collagen- or U46619-induced rat platelet rich plasma (PRP). Treatment with Wnt5a to U46619- stimulated PRP resulted in an increase in the level of phosphorylated Akt, whereas phosphorylation of PKC? and JNK1 was unaffected. In addition, inhibition of PI3K blocked the potentiating effect of Wnt5a. Taken together, these results suggest that Wnt5a potentiates U46619-induced platelet aggregation via the PI3K/Akt pathway.
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KEYWORD
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Akt1, platelet aggregation, platelet-rich plasma, U46619, Wnt
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