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Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow
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. Usin...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Higher Education Press
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291781/ https://www.ncbi.nlm.nih.gov/pubmed/28097631 http://dx.doi.org/10.1007/s13238-016-0364-4 |
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author | Huang, Bing Ling, Yingchen Lin, Jiangguo Du, Xin Fang, Ying Wu, Jianhua |
author_facet | Huang, Bing Ling, Yingchen Lin, Jiangguo Du, Xin Fang, Ying Wu, Jianhua |
author_sort | Huang, Bing |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5291781 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Higher Education Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-52917812017-02-16 Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow Huang, Bing Ling, Yingchen Lin, Jiangguo Du, Xin Fang, Ying Wu, Jianhua Protein Cell Research Article 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. Higher Education Press 2017-01-18 2017-02 /pmc/articles/PMC5291781/ /pubmed/28097631 http://dx.doi.org/10.1007/s13238-016-0364-4 Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Research Article Huang, Bing Ling, Yingchen Lin, Jiangguo Du, Xin Fang, Ying Wu, Jianhua Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow |
title | Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow |
title_full | Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow |
title_fullStr | Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow |
title_full_unstemmed | Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow |
title_short | Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow |
title_sort | force-dependent calcium signaling and its pathway of human neutrophils on p-selectin in flow |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291781/ https://www.ncbi.nlm.nih.gov/pubmed/28097631 http://dx.doi.org/10.1007/s13238-016-0364-4 |
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