PTEN regulates collagen-induced platelet activation

• Published in: Blood 2010-10, Vol.116 (14), p.2579-2581
• Main Authors: Weng, Zhen, Li, Ding, Zhang, Lin, Chen, Jian, Ruan, Changgeng, Chen, Guoqiang, Gartner, T. Kent, Liu, Junling
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Platelets - metabolism; Collagen - metabolism; Gene Deletion; Hematologic and hematopoietic diseases; Medical sciences; Mice; Mice, Inbred C57BL; Phosphatidylinositol 3-Kinases - metabolism; Platelet Activation; PTEN Phosphohydrolase - genetics; PTEN Phosphohydrolase - metabolism
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood-2010-03-277236

Phosphatidylinositol 3-kinase (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, indomethacin + 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.