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补体片段 C3a 控制细胞集体迁移过程中的细胞间相互吸引。

Complement fragment C3a controls mutual cell attraction during collective cell migration.

机构信息

Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK.

出版信息

Dev Cell. 2011 Dec 13;21(6):1026-37. doi: 10.1016/j.devcel.2011.10.012. Epub 2011 Nov 24.

DOI:10.1016/j.devcel.2011.10.012
PMID:22118769
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3272547/
Abstract

Collective cell migration is a mode of movement crucial for morphogenesis and cancer metastasis. However, little is known about how migratory cells coordinate collectively. Here we show that mutual cell-cell attraction (named here coattraction) is required to maintain cohesive clusters of migrating mesenchymal cells. Coattraction can counterbalance the natural tendency of cells to disperse via mechanisms such as contact inhibition and epithelial-to-mesenchymal transition. Neural crest cells are coattracted via the complement fragment C3a and its receptor C3aR, revealing an unexpected role of complement proteins in early vertebrate development. Loss of coattraction disrupts collective and coordinated movements of these cells. We propose that coattraction and contact inhibition act in concert to allow cell collectives to self-organize and respond efficiently to external signals, such as chemoattractants and repellents.

摘要

细胞集体迁移是一种对于形态发生和癌症转移至关重要的运动模式。然而,对于迁移细胞如何集体协调,人们知之甚少。在这里,我们表明,相互的细胞间吸引力(在这里称为共吸引)是维持迁移间充质细胞凝聚簇所必需的。共吸引可以通过接触抑制和上皮-间充质转化等机制来平衡细胞自然分散的趋势。神经嵴细胞通过补体片段 C3a 和其受体 C3aR 进行共吸引,揭示了补体蛋白在早期脊椎动物发育中的一个意外作用。共吸引的丧失会破坏这些细胞的集体和协调运动。我们提出,共吸引和接触抑制协同作用,使细胞集体能够自我组织,并有效地对外部信号(如趋化因子和排斥剂)做出反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/9ad0d2889b01/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/c3ded85cb84b/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/984051036b6a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/18b709b4df23/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/cfddc6d3298f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/6dd01987b29d/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/8eee2f85f69a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/0adf4af185ed/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/9ad0d2889b01/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/c3ded85cb84b/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/984051036b6a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/18b709b4df23/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/cfddc6d3298f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/6dd01987b29d/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/8eee2f85f69a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/0adf4af185ed/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f28e/3272547/9ad0d2889b01/gr7.jpg

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