细胞生物学
趋化因子
细胞迁移
趋化因子受体
运动性
归巢(生物学)
染色质
生物
细胞
化学
免疫学
炎症
生物化学
生态学
DNA
作者
Bianca Calì,Mathieu Deygas,Fabio Munari,Elisabetta Marcuzzi,Antonino Cassará,Lara Toffali,Massimo Vetralla,Mathilde Bernard,Matthieu Piel,Onelia Gagliano,Marta Mastrogiovanni,Carlo Laudanna,Nicola Elvassore,Barbara Molon,Pablo Agustín Vargas,Antonella Viola
出处
期刊:Science Signaling
[American Association for the Advancement of Science (AAAS)]
日期:2022-11-22
卷期号:15 (761)
被引量:6
标识
DOI:10.1126/scisignal.abk2552
摘要
To reach inflamed tissues from the circulation, neutrophils must overcome physical constraints imposed by the tissue architecture, such as the endothelial barrier or the three-dimensional (3D) interstitial space. In these microenvironments, neutrophils are forced to migrate through spaces smaller than their own diameter. One of the main challenges for cell passage through narrow gaps is the deformation of the nucleus, the largest and stiffest organelle in cells. Here, we showed that chemokines, the extracellular signals that guide cell migration in vivo, modulated nuclear plasticity to support neutrophil migration in restricted microenvironments. Exploiting microfabricated devices, we found that the CXC chemokine CXCL12 enhanced the nuclear pliability of mouse bone marrow-derived neutrophils to sustain their migration in 3D landscapes. This previously uncharacterized function of CXCL12 was mediated by the atypical chemokine receptor ACKR3 (also known as CXCR7), required protein kinase A (PKA) activity, and induced chromatin compaction, which resulted in enhanced cell migration in 3D. Thus, we propose that chemical cues regulate the nuclear plasticity of migrating leukocytes to optimize their motility in restricted microenvironments.
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