Blood:AMPK-ACC信号通路可调节血小板磷脂含量、增强血小板功能、促进血栓形成

2018-07-19 MedSci MedSci原创

中心点:在血小板中,AMPK-ACC信号通路是调节原发性止血和动脉血栓形成的关键机制。AMPK-ACC信号可通过调节血小板磷脂含量来调控胶原蛋白诱导的花生四烯酸(TXA2)合成、致密颗粒释放。摘要:在凝血酶或胶原蛋白的刺激下,血小板中的AMP-活化蛋白激酶(AMPK)α1被激活,发生磷酸化,进而抑制乙酰CoA羧化酶(ACC)。鉴于ACC对于脂肪酸合成至关重要,而脂肪酸对血小板激活又必不可少,因此,

中心点:

在血小板中,AMPK-ACC信号通路是调节原发性止血和动脉血栓形成的关键机制。

AMPK-ACC信号可通过调节血小板磷脂含量来调控胶原蛋白诱导的花生四烯酸(TXA2)合成、致密颗粒释放。

摘要:

在凝血酶或胶原蛋白的刺激下,血小板中的AMP-活化蛋白激酶(AMPK)α1被激活,发生磷酸化,进而抑制乙酰CoA羧化酶(ACC)。

鉴于ACC对于脂肪酸合成至关重要,而脂肪酸对血小板激活又必不可少,因此,研究人员推测ACC对血小板的功能具有重要的调节作用。为验证该推测,研究人员采用双重敲入(DKI)的小鼠模型,即将AMPK磷酸化位点(ACC1上的Ser79和ACC2上的Ser212)突变掉,以阻断AMPK信号传递至ACC。

抑制ACC磷酸化会促进活体上损伤诱导的动脉血栓形成,并增强胶原图层表面的血栓形成。在胶原蛋白的刺激下,AMPK-ACC信号通路缺失可增加血栓素的生成、促进致密颗粒分泌。ACC DKI血小板的含有花生四烯酸的磷脂酰乙醇胺缩圈磷脂脂质增多。

综上所述,受到胶原蛋白刺激时,AMPK-ACC信号通路可通过特异性调节血栓素和颗粒释放与血栓形成调控相偶联;该过程可能是通过增加血小板激活的关键调节因子——花生四烯酸合成所需要的血小板磷脂含量而实现的。

原始出处:

Sophie Lepropre,et al. AMPK-ACC signaling modulates platelet phospholipids content and potentiates platelet function and thrombus formation. Blood  2018  :blood-2018-02-831503;  doi: https://doi.org/10.1182/blood-2018-02-831503

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    2018-07-20 明崖

    学习了,有用的研究

    0

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    2018-07-20 惠映实验室

    学习了,谢谢分享。

    0

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