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PTEN regulates collagen-induced platelet activation
Zhen Weng1, Ding Li1, Lin Zhang1, Jian Chen2, Changgeng Ruan3, Guoqiang Chen4, T. Kent Gartner5 and Junling Liu1,*
1 Department of Biochemistry and Molecular & Cell Biology, Institute of Medical Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China; 2 Intensive Care Unit, Xinjiang Traditional Chinese Medicine Hospital, Xinjiang Medical University, Xinjiang, China; 3 China Key Laboratory of Thrombosis and Hemostasis of Ministry of Health, The First Affiliated Hospital of Soochow University, Suzhou, China; 4 Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China; 5 Department of Biology, University of Memphis, Memphis, TN, United States
PI3K has been shown to play an important role in collagen-induced platelet activation, but the role(s) of PTEN, a major regulator of the PI3K/Akt signaling pathway, has not been examined in platelets. Here, we report that PTEN-/- mouse blood contains 25% more platelets than PTEN+/+ blood, and that PTEN deficiency significantly shortened the bleeding time, increased the sensitivity of platelets to collagen-induced activation and aggregation, and enhanced phosphorylation of Akt at Ser473 in response to collagen. Furthermore, we found that PP2, and the combination of apyrase, indomethcin+1B5, respectively inhibited collagen-induced aggregation in both PTEN+/+ and PTEN-/- platelets. In contrast, LY294002 (a PI3K inhibitor) prevented the aggregation of PTEN+/+, but not PTEN-/- platelets. Therefore, PTEN apparently regulates collagen-induced platelet activation through PI3K/Akt dependent and independent signaling pathways.
