Mechanical features of endothelium regulate cell adhesive molecule-induced calcium response in neutrophils
文献类型:期刊论文
作者 | Xu YH(徐艳红); Huang DD(黄丹丹); Lv SQ(吕守芹)![]() ![]() ![]() |
刊名 | APL BIOENGINEERING
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出版日期 | 2019-03 |
卷号 | 3页码:16104 |
ISSN号 | 2473-2877 |
DOI | 10.1063/1.5045115 |
英文摘要 | Atherosclerosis is caused by chronic inflammation associated with the adhesion of neutrophils and endothelial cells (ECs) that is mediated by their respective cellular adhesive molecules to stiffened blood vessel walls. However, the stiffness dependence of calcium flux on neutrophils remains unclear yet. Here, the effect of substrate stiffness by ECs on neutrophils' calcium spike was quantified when the individual neutrophils that adhered to the human umbilical vascular endothelial cell (HUVEC) monolayer were pre-placed onto a stiffness-varied polyacrylamide substrate (5 or 34.88 kPa) or glass surface. Our data indicated that E-/P-selectins and intercellular adhesion molecule 1 (ICAM-1) on HUVECs and beta(2)-integrins, P-selectin glycoprotein ligand 1 (PSGL-1), and CD44s on neutrophils were all involved in mediating neutrophil calcium spike in a stiffness-dependent manner, in which the increase in substrate stiffness enhanced the calcium intensity and the oscillation frequency (spike number). Such stiffness-dependent calcium response is associated with the induced selectin related to beta(2)-integrin activation through the Syk/Src signaling pathway, and F-actin/myosin II are also involved in this. Moreover, tension-activated calcium ion channels displayed critical roles in initiating stiffness-dependent calcium spike. These results provide an insight into understanding how the stiffening of vascular walls could regulate the calcium flux of adhered neutrophils, and thus the immune responses in atherosclerosis. (C) 2019 Author(s). |
学科主题 | Engineering, Biomedical |
分类号 | 二类/Q1 |
语种 | 英语 |
WOS记录号 | WOS:000462879400008 |
资助机构 | National Natural Science Foundation of China [31627804, 91642203, 11772345, 91539119] ; Chinese Academy of Sciences Strategic Priority Research Program [XDB22040101] ; Frontier Science Key Project [QYZDJ-SSW-JSC018] |
其他责任者 | Zhang, Y ; Long, M (corresponding author), Chinese Acad Sci, Inst Mech, Ctr Biomech & Bioengn, Beijing 100190, Peoples R China. ; Zhang, Y ; Long, M (corresponding author), Chinese Acad Sci, Inst Mech, Key Lab Micrograv, Natl Micrograv Lab, Beijing 100190, Peoples R China. ; Zhang, Y ; Long, M (corresponding author), Chinese Acad Sci, Beijing Key Lab Engn Construct & Mechanobiol, Inst Mech, Beijing 100190, Peoples R China. ; Zhang, Y ; Long, M (corresponding author), Univ Chinese Acad Sci, Sch Engn Sci, Beijing 100049, Peoples R China. |
源URL | [http://dspace.imech.ac.cn/handle/311007/90260] ![]() |
专题 | 力学研究所_国家微重力实验室 |
作者单位 | 1.Univ Chinese Acad Sci, Sch Engn Sci, Beijing 100049, Peoples R China 2.Chinese Acad Sci, Beijing Key Lab Engn Construct & Mechanobiol, Inst Mech, Beijing 100190, Peoples R China 3.Chinese Acad Sci, Inst Mech, Key Lab Micrograv, Natl Micrograv Lab, Beijing 100190, Peoples R China 4.Chinese Acad Sci, Inst Mech, Ctr Biomech & Bioengn, Beijing 100190, Peoples R China |
推荐引用方式 GB/T 7714 | Xu YH,Huang DD,Lv SQ,et al. Mechanical features of endothelium regulate cell adhesive molecule-induced calcium response in neutrophils[J]. APL BIOENGINEERING, 1,2019,3:16104. |
APA | 徐艳红,黄丹丹,吕守芹,章燕,&龙勉.(2019).Mechanical features of endothelium regulate cell adhesive molecule-induced calcium response in neutrophils.APL BIOENGINEERING,3,16104. |
MLA | 徐艳红,et al."Mechanical features of endothelium regulate cell adhesive molecule-induced calcium response in neutrophils".APL BIOENGINEERING 3(2019):16104. |
入库方式: OAI收割
来源:力学研究所
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