Role for plastin in host defense distinguishes integrin signaling from cell adhesion and spreading
Role for plastin in host defense distinguishes integrin signaling from cell adhesion and spreading
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DOI：
10.1016/s1074-7613(03)00172-9
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发表时间：
2003-07-01
期刊：
影响因子：
32.4
通讯作者：
Brown, EJ
中科院分区：
文献类型：
--
作者：
Chen, H;Mocsai, A;Brown, EJ
整合素连接激活细胞黏附和信号转导，部分是通过肌动蛋白细胞骨架的重组。Plstins(也称为纤毛蛋白)是存在于所有细胞中的皮质细胞骨架的肌动蛋白交联蛋白，从酵母到哺乳动物都是如此。在这里，我们表明，尽管吞噬功能正常，但在体内和体外，缺乏纤溶酶缺乏的中性粒细胞(PMN)在杀死细菌病原体金黄色葡萄球菌方面是不足的。与整合素β2缺乏的PMN一样，由于整合素依赖的SYK活性显著降低，纤溶酶缺乏的PMN不能产生黏附依赖性呼吸爆发。与β2(-/-)中性粒细胞不同，缺乏纤溶酶的中性粒细胞可以正常黏附和扩散。因此，缺乏纤溶酶使经典的整合素受体的黏附和扩散功能从细胞内信号转导中分离出来。
Integrin ligation activates both cell adhesion and signal transduction, in part through reorganization of the actin cytoskeleton. Plastins (also known as fimbrins) are actin-crosslinking proteins of the cortical cytoskeleton present in all cells and conserved from yeast to mammals. Here we show that plastin-deficient polymorphonuclear neutrophils (PMN) are deficient in killing the bacterial pathogen Staphylococcus aureus in vivo and in vitro, despite normal phagocytosis. Like integrin beta2-deficient PMN, plastin-deficient PMN cannot generate an adhesion-dependent respiratory burst, because of markedly diminished integrin-dependent syk activation. Unlike beta2(-/-) PMN, plastin-deficient PMN adhere and spread normally. Deficiency of plastin thus separates the classical integrin receptor functions of adhesion and spreading from intracellular signal transduction.