Direct observation and quantification of macrophage chemoattraction to the growth factor CSF-1.
Direct observation and quantification of macrophage chemoattraction to the growth factor CSF-1.
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发表时间：
1996-04
影响因子：
4
通讯作者：
Sarah E. Webb;Jeffrey W. Pollard;Gareth E. Jones
中科院分区：
文献类型：
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作者：
Sarah E. Webb;Jeffrey W. Pollard;Gareth E. Jones
克隆的小鼠巨噬细胞系BAC1.25F与原代巨噬细胞相似，因为它依赖集落刺激因子-1(CSF-1)来维持生存和增殖。将CSF-1重新添加到被广泛组织的F-肌动蛋白包围的细胞因子剥夺的细胞中，刺激细胞快速扩散和细胞极化。使用Dunn趋化小室监测刺激的巨噬细胞在2小时内的运动。用1.32 nM人重组CSF-1重新刺激的细胞以平均每小时7.71微米的速度迁移，但没有显示出定向偏爱。在线性浓度梯度的CSF-1中，被剥夺细胞因子的细胞再次被刺激迁移，细胞平均运动速率为6.88微米/小时，与在各向同性环境中测量的结果没有显著差异。然而，细胞有强烈的定向倾向，使它们的长轴与CSF-1的梯度一致，并优先向CSF-1的来源迁移。荧光蛋白共聚焦成像显示，迁移细胞的前板内含有丰富的F-肌动蛋白，但肌动蛋白没有排列成应力纤维样结构。这些数据支持CSF-1对巨噬细胞既是趋化因子又是趋化因子的命题。肿瘤坏死因子(TNF-α)不能刺激细胞迁移，因此既不是趋化因子，也不是趋化因子。然而，暴露在肿瘤坏死因子-α和脑脊液-1双重浓度梯度下的细胞确实成功迁移，尽管对脑脊液-1的趋化反应被取消。
The cloned mouse macrophage cell line, BAC1.25F, resembles primary macrophages in its dependence on colony stimulating factor-1 (CSF-1) for both viability and proliferation. Re-addition of CSF-1 to cytokine-deprived cells, which are rounded with diffusely organised F-actin, stimulates rapid cell spreading and cell polarisation. Using the Dunn chemotaxis chamber the movement of stimulated macrophages was monitored over a 2 hour period. Cells restimulated with 1.32 nM human recombinant CSF-1 migrated at a mean rate of 7.71 microns per hour, but showed no directional preferences. In a linear concentration gradient of CSF-1, cytokine-deprived cells were again stimulated to migrate and the mean rate of cell motility, at 6.88 microns per hour, was not significantly different from that measured in an isotropic environment of CSF-1. However, there was a strong preference for the cells to orientate so that their long axes aligned with the CSF-1 gradient and they migrated preferentially towards the source of CSF-1. Migrating cells contained abundant F-actin within the leading lamellae as judged by confocal imaging of fluorescent phalloidin, but the actin was not arranged into stress fibre-like structures. These data support the proposition that CSF-1 is both a chemokinetic and chemotactic agent for macrophages. Tumour necrosis factor (TNF-alpha) failed to stimulate cell migration and thus was neither chemokinetic nor a chemotactic agent. However, cells exposed to a dual concentration gradient of both TNF-alpha and CSF-1 did migrate successfully, although the chemotactic response to CSF-1 was abolished.