Molecules and Cells

, 32:333

Wnt5a Potentiates U46619-Induced platelet aggregation via the PI3K/Akt pathway

  • Sun Young Kim
  • Sewoon Kim
  • Hye Sook Yun-Choi
  • Eek-hoon Jho
Article

DOI: 10.1007/s10059-011-0134-3

Cite this article as:
Kim, S.Y., Kim, S., Yun-Choi, H.S. et al. Mol Cells (2011) 32: 333. doi:10.1007/s10059-011-0134-3

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.

Keywords

Akt1 platelet aggregation platelet-rich plasma U46619 Wnt 

Copyright information

© The Korean Society for Molecular and Cellular Biology and Springer Netherlands 2011

Authors and Affiliations

  • Sun Young Kim
    • 1
  • Sewoon Kim
    • 2
  • Hye Sook Yun-Choi
    • 1
  • Eek-hoon Jho
    • 2
  1. 1.Natural Products Research Institute, College of PharmacySeoul National UniversitySeoulKorea
  2. 2.Department of Life ScienceUniversity of SeoulSeoulKorea