Blood:细胞保护性活化蛋白C可通过mTORC1抑制来预防NIrp3炎性小体诱导的缺血再灌注损伤。

2017-09-08 qinqiyun MedSci原创

aPC在IRI后的细胞保护作用与凋亡抑制相关。IRI是由炎症引起的,因此从概念上讲,细胞死亡形式从免疫沉默的细胞凋亡中分离出来更有可能是相关的。炎性小体激活导致的细胞死亡,是在IRI中观察到典型的细胞死亡类型,研究人员推测,aPC可通过抑制炎性小体活性来改善IRI。

中心点:

活化蛋白C(aPC)通过抑制mTORC1介导的NIrp3炎性小体的激活来保护心肌细胞和肾脏缺血再灌注损伤(IRI)。

NIrp3炎症体受aPC抑制是不依赖其抗凝血作用,而且依赖PAR1,而且可被parmodulin-2模拟。

摘要:

aPC在IRI后的细胞保护作用与凋亡抑制相关。IRI是由炎症引起的,因此从概念上讲,细胞死亡形式从免疫沉默的细胞凋亡中分离出来更有可能是相关的。炎性小体激活导致的细胞死亡,是在IRI中观察到典型的细胞死亡类型,研究人员推测,aPC可通过抑制炎性小体活性来改善IRI。

研究人员对aPC在心肌细胞和肾脏IRI中对炎性小体活性的影响进行分析。在小鼠心肌IRI后予以aPC治疗可减小心肌梗死的面积和降低NIrp炎性小体的活性。

体内动力学分析表明NIrp炎性小体激活发生在心肌细胞损伤核凋亡之前,证实NIrp3炎性小体的病理上的作用。持续性活化的NIrp3A350V突变可消除aPC的保护作用,表明aPC介导的IRI保护作用是通过抑制NIrp3。

体外试验中,aPC通过PAR-1和mTORC1信号通路抑制巨噬细胞、心肌细胞和心肌纤维细胞的炎性小体活化。

因此,在心肌细胞IRI中,抑制PAR-1信号通路,但不抑制aPC的抗凝作用,可消除aPC抑制NIrp3炎性小体活性和组织损伤的能力。

通过parmodulin-2以PAR-1信号通路为基础的靶向治疗,抑制mTORC1和NIrp3炎性小体活性和改善心肌细胞IRI的效果,与aPC相似。肾脏IRI证实了aPC介导的Nlrp3炎性小体抑制的相关性,在肾脏IRI中,aPC也是依赖于NIrp3炎性小体抑制发挥组织保护性作用。

本研究结果表明aPC通过抑制mTORC1依赖性炎性小体活化发挥组织缺血再灌注损伤的保护作用,而且,可用parmodulins模拟aPC-PAR1信号通路或许课用于治疗IRI。

原始出处:

Sumra Nazir,et al.Cytoprotective activated protein C averts Nlrp3 inflammasome induced ischemia reperfusion injury via mTORC1 inhibition.Blood. September 07,2017.https://doi.org/10.1182/blood-2017-05-782102

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    2017-09-10 雕雕
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    2017-09-08 184****9840

    学习了受益匪浅

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