细胞生物学
整合素
细胞迁移
趋化性
细胞骨架
焦点粘着
整合素αM
肌球蛋白
细胞粘附
趋化因子
粘附
细胞
生物
材料科学
免疫学
免疫系统
信号转导
生物化学
受体
复合材料
作者
Wenhui Hu,Wenbo Gao,Yixin Gong,Pan Guo,Wang Li,Xinyu Shu,Shouqin Lü,Zhu Zeng,Yan Zhang,Mian Long
标识
DOI:10.1021/acsami.3c00288
摘要
Migrating neutrophils are found to leave behind subcellular trails in vivo, but the underlying mechanisms remain unclear. Here, an in vitro cell migration test plus an in vivo observation was applied to monitor neutrophil migration on intercellular cell adhesion molecule-1 (ICAM-1) presenting surfaces. Results indicated that migrating neutrophils left behind long-lasting, chemokine-containing trails. Trail formation tended to alleviate excessive cell adhesion enhanced by the trans-binding antibody and maintain efficient cell migration, which was associated with differential instantaneous edge velocity between the cell front and rear. CD11a and CD11b worked differently in inducing trail formation with polarized distributions on the cell body and uropod. Trail release at the cell rear was attributed to membrane ripping, in which β2-integrin was disrupted from the cell membrane through myosin-mediated rear contraction and integrin–cytoskeleton dissociation, potentiating a specialized strategy of integrin loss and cell deadhesion to maintain efficient migration. Moreover, neutrophil trails left on the substrate served as immune forerunners to recruit dendritic cells. These results provided an insight in elucidating the mechanisms of neutrophil trail formation and deciphering the roles of trail formation in efficient neutrophil migration.
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