Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow

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• 作者：Bing Huang ; Yingchen Ling ; Jiangguo Lin ; Xin Du ; Ying Fang ; Jianhua Wu
• 关键词：neutrophils ; P ; selectin ; calcium signaling ; shear stress
• 刊名：Protein & Cell
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：8
• 期：2
• 页码：103-113
• 全文大小：1174KB
• 刊物主题：Biochemistry, general; Protein Science; Cell Biology; Stem Cells; Human Genetics; Developmental Biology;
• 出版者：Higher Education Press
• ISSN：1674-8018
• 卷排序：8

文摘

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.