Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow.
Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow.
复制标题
流中人中性粒细胞对 P-选择素的力依赖性钙信号传导及其通路
DOI：
10.1007/s13238-016-0364-4
复制
发表时间：
2017-02
期刊：
影响因子：
21.1
通讯作者：
Wu J
中科院分区：
文献类型：
--
作者：
Huang B;Ling Y;Lin J;Du X;Fang Y;Wu J
P-selectin engagement of P-selectin glycoprotein ligand-1 (PSGL-1) causes circulating leukocytes to roll on and adhere to the vascular surface, and mediates intracellular calcium flux, a key but unclear event for subsequent arresting firmly at and migrating into the infection or injured tissue. Using a parallel plate flow chamber technique and intracellular calcium ion detector (Fluo-4 AM), the intracellular calcium flux of firmly adhered neutrophils on immobilized P-selectin in the absence of chemokines at various wall shear stresses was investigated here in real time by fluorescence microscopy. The results demonstrated that P-selectin engagement of PSGL-1 induced the intracellular calcium flux of firmly adhered neutrophils in flow, increasing P-selectin concentration enhanced cellular calcium signaling, and, force triggered, enhanced and quickened the cytoplasmic calcium bursting of neutrophils on immobilized P-selectin. This P-selectin-induced calcium signaling should come from intracellular calcium release rather than extracellular calcium influx, and be along the mechano-chemical signal pathway involving the cytoskeleton, moesin and Spleen tyrosine kinase (Syk). These results provide a novel insight into the mechano-chemical regulation mechanism for P-selectin-induced calcium signaling of neutrophils in flow.
