Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow.
10.1007/s13238-016-0364-4
- Author:
Bing HUANG
1
;
Yingchen LING
1
;
Jiangguo LIN
1
;
Xin DU
2
;
Ying FANG
3
;
Jianhua WU
4
Author Information
1. School of Bioscience & Bioengineering, South China University of Technology, Guangzhou, 510006, China.
2. Hematology and Oncology Division, Guangdong General Hospital, Guangzhou, 510080, China.
3. School of Bioscience & Bioengineering, South China University of Technology, Guangzhou, 510006, China. yfang@scut.edu.cn.
4. School of Bioscience & Bioengineering, South China University of Technology, Guangzhou, 510006, China. wujianhua@scut.edu.cn.
- Publication Type:Journal Article
- Keywords:
P-selectin;
calcium signaling;
neutrophils;
shear stress
- MeSH:
Calcium Signaling;
Female;
Humans;
Male;
Membrane Glycoproteins;
metabolism;
Neutrophils;
metabolism;
P-Selectin;
metabolism;
Stress, Mechanical;
Syk Kinase;
metabolism
- From:
Protein & Cell
2017;8(2):103-113
- CountryChina
- Language:English
-
Abstract:
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.
