PTEN regulates collagen-induced platelet activation

被引：63

作者：

Weng, Zhen ^{[1
]}

Li, Ding ^{[1
]}

Zhang, Lin ^{[1
]}

Chen, Jian ^{[2
]}

Ruan, Changgeng ^{[3
]}

Chen, Guoqiang ^{[4
]}

Gartner, T. Kent ^{[5
]}

Liu, Junling ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Dept Biochem & Mol & Cell Biol, Key Lab Cell Differentiat & Apoptosis Chinese, Inst Med Sci,Sch Med,Minist Educ, Shanghai 200025, Peoples R China

[2] Xinjiang Med Univ, Xinjiang Tradit Chinese Med Hosp, Intens Care Unit, Xinjiang, Peoples R China

[3] Soochow Univ, Affiliated Hosp 1, China Key Lab Thrombosis & Hemostasis, Jiangsu Inst Hematol,Minist Hlth, Suzhou, Peoples R China

[4] Shanghai Jiao Tong Univ, Dept Pathophysiol, Key Lab Cell Differentiat & Apoptosis Chinese, Minist Educ,Sch Med, Shanghai 200025, Peoples R China

[5] Univ Memphis, Dept Biol, Memphis, TN 38152 USA

来源：

BLOOD | 2010年 / 116卷 / 14期

关键词：

HEMATOPOIETIC STEM-CELLS; GLYCOPROTEIN-VI; IN-VIVO; PATHWAY;

D O I：

10.1182/blood-2010-03-277236

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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. (Blood. 2010;116(14):2579-2581)

引用

页码：2579 / 2581

页数：3

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