Wnt5a Potentiates U46619-Induced platelet aggregation <Emphasis Type="Italic">via</Emphasis> the PI3K/Akt pathway |
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Authors: | Sun Young Kim Sewoon Kim Hye Sook Yun-Choi Eek-hoon Jho |
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Institution: | Natural Products Research Institute, College of Pharmacy, Seoul National University, Seoul 151-742, Korea. |
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Abstract: | Platelet aggregation plays crucial roles in the formation of hemostatic plugs and thrombosis. Although it was recently 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 PKCδ 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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Keywords: | Akt1 platelet aggregation platelet-rich plasma U46619 Wnt |
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