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首页> 外文期刊>Cell and Tissue Research >Plerixafor induces the rapid and transient release of stromal cell-derived factor-1 alpha from human mesenchymal stromal cells and influences the migration behavior of human hematopoietic progenitor cells
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Plerixafor induces the rapid and transient release of stromal cell-derived factor-1 alpha from human mesenchymal stromal cells and influences the migration behavior of human hematopoietic progenitor cells

机译：Plerixafor诱导人间充质基质细胞中基质细胞衍生因子-1α的快速瞬时释放，并影响人类造血祖细胞的迁移行为

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摘要

The interaction between the stromal cell-derived factor-1 alpha (SDF-1α, CXCL12) and its chemokine receptor CXCR4 has been reported to regulate stem cell migration, mobilization and homing. The CXCR4 antagonist plerixafor is highly efficient in mobilizing hematopoietic progenitor cells (HPCs). However, the precise regulatory mechanisms governing the CXCR4/SDF-1α axis between the bone marrow niche and HPCs remain unclear. In this study, we quantify the impact of plerixafor on the interaction between human bone marrow derived mesenchymal stromal cells (MSCs) and human CD34+ HPCs. An assessment of SDF-1α levels in the supernatant of MSC cultures revealed that exposure to plerixafor led to a transient increase but had no long-term effect. In Transwell experiments, we observed that the addition of SDF-1α significantly stimulated HPC migration; this stimulation was almost completely antagonized by the addition of plerixafor, confirming the direct impact of the CXCR4/SDF-1α interaction on the migration capacity of HPCs. We also developed a new microstructural niche model to determine the chemotactic sensitivity of HPCs. Time-lapse microscopy demonstrated that HPCs migrated actively along an SDF-1α gradient within the microchannels and the quantitative assessment of the required minimum gradient initiating this chemotaxis revealed a surprisingly high sensitivity of HPCs. These data demonstrate the fine-tuned balance of the CXCR4/SDF-1α axis and the synergistic effects of plerixafor on HPCs and MSCs, which most likely represent the key mechanisms for the consecutive mobilization of HPCs from the bone marrow niche into the circulating blood.
机译：据报道，基质细胞衍生因子-1α（SDF-1α，CXCL12）与其趋化因子受体CXCR4之间的相互作用调节干细胞的迁移，动员和归巢。 CXCR4拮抗剂plerixafor在动员造血祖细胞（HPC）方面非常高效。但是，尚不清楚控制骨髓小生境和HPC之间的CXCR4 /SDF-1α轴的精确调控机制。在这项研究中，我们量化了plerixafor对人骨髓来源的间充质基质细胞（MSCs）与人CD34 + HPC之间相互作用的影响。对MSC培养物上清液中SDF-1α水平的评估表明，暴露于plerixafor会导致短暂增加，但没有长期影响。在Transwell实验中，我们观察到SDF-1α的添加显着刺激了HPC迁移。通过添加plerixafor，这种刺激几乎完全被拮抗，证实了CXCR4 /SDF-1α相互作用对HPC迁移能力的直接影响。我们还开发了一种新的微结构生态位模型，以确定HPC的趋化敏感性。延时显微镜显示，HPC在微通道内沿SDF-1α梯度活跃迁移，对启动该趋化性所需的最小梯度的定量评估显示，HPC出乎意料的高灵敏度。这些数据证明了CXCR4 /SDF-1α轴的微调平衡以及plerixafor对HPC和MSC的协同作用，这很可能代表了HPC从骨髓生境连续动员到循环血液中的关键机制。

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