Effect of 0.4 mT power frequency magnetic field on the migration of human amniotic epithelial cells

Fan YANG; He LIU; Hongxin QI; Jie ZHANG; Ruohong XIA; Xianghui WANG

doi:10.11889/j.1000-3436.2018.rrj.36.030202

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Effect of 0.4 mT power frequency magnetic field on the migration of human amniotic epithelial cells

RADIOBIOLOGY AND RADIOMEDICINE | 更新时间：2021-12-10

- Effect of 0.4 mT power frequency magnetic field on the migration of human amniotic epithelial cells
- Journal of Radiation Research and Radiation Processing Vol. 36, Issue 3, (2018)
- 作者机构：
  
  1.华东师范大学物理与材料科学学院生物物理实验室上海 200241
- 作者简介：
- 基金信息：
  
  National Program on Key Basic Research Project (973 program)(2011CB503703)
- DOI：10.11889/j.1000-3436.2018.rrj.36.030202
  CLC：
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Fan YANG, He LIU, Hongxin QI, et al. Effect of 0.4 mT power frequency magnetic field on the migration of human amniotic epithelial cells. [J]. Journal of Radiation Research and Radiation Processing 36(3):030202-12(2018)
DOI：

Fan YANG, He LIU, Hongxin QI, et al. Effect of 0.4 mT power frequency magnetic field on the migration of human amniotic epithelial cells. [J]. Journal of Radiation Research and Radiation Processing 36(3):030202-12(2018) DOI： 10.11889/j.1000-3436.2018.rrj.36.030202.

摘要

探讨了0.4 mT工频磁场（Power frequency magnetic field，PFMF）暴露影响人羊膜成纤维（Human amniotic epithelial，FL）细胞迁移的分子机制。利用免疫荧光染色和western blotting方法检测了磁场暴露对FL细胞内黏着斑调控蛋白黏着斑激酶（Focal adhesion kinase，FAK）、桩蛋白（Paxillin）的分布、含量和部分关键活性蛋白的影响；通过细胞划痕实验，验证了磁场通过激活FAK从而激活细胞的迁移反应。结果表明：相较于对照组，PFMF暴露导致黏着斑总数量上升，并诱导信号蛋白FAK与桩蛋白更集中地分布在细胞边缘处，导致桩蛋白的总含量增加；FAK蛋白总含量无显著性变化，但其Y397磷酸化水平明显上调；用PD153035（PD）抑制表皮生长因子受体（Epidermal growth factor receptor，EGFR）的活性，或用FAK Inhibitor 14（FI）抑制Y397-FAK磷酸化，PFMF或表皮生长因子（Epidermal growth factor，EGF）引起的上述现象均消失；细胞划痕实验结果显示，PFMF促进了细胞的迁移，但当Y397-FAK被FI抑制后，PFMF对细胞迁移的促进效果几乎全部消失；PFMF引发的这些变化均与EGFR的配体EGF对细胞迁移产生的效果类似。0.4 mT工频磁场通过激活EGFR而激活黏着斑信号通路中的FAK、桩蛋白，调控黏着斑的形成与分布，在细胞前端协助片状伪足的延展，从而诱发细胞迁移。

Abstract

To study the molecular mechanism of the effect of a 0.4 mT power frequency magnetic field (PFMF) on the mobility of human amniotic epithelial (FL) cells, immunofluorescence labeling and western blotting were used to detect the distribution, expression, and activity of two key regulatory proteins, FAK and Paxillin, which function in the focal adhesion signaling pathway. Subsequently, cell migration was evaluated to verify whether FAK participated in PFMF-activated cell migration. The results showed that compared to the sham group, the number of FAK and Paxillin foci in the MF group increased at cell borders, which implied that the total number of focal adhesion spots had increased. Moreover, the total content of Paxillin increased in the PFMF-exposed group. Although the levels of FAK were not significantly changed, Y397 phosphorylation of FAK was significantly upregulated. When the activity of the epidermal growth factor receptor (EGFR) was inhibited by PD153035 (PD), or the phosphorylation of Y397-FAK was inhibited by FAK Inhibitor 14 (FI), the above-mentioned effects were no longer seen. Cell migration experiments showed that PFMF promoted cell migration through upregulating the FAK phosphorylation level, because the effect was sensitive to the inhibition of Y397-FAK phosphorylation. All evidence indicated that the effect of PFMF on cell mobility was similar to that of the EGFR ligand, epidermal growth factor (EGF). Therefore, it can be concluded that 0.4 mT PFMF regulates the formation and distribution of focal adhesions by activating EGFR, which subsequently activates FAK and Paxillin, resulting in an increase in cell mobility via lamellipodial extension.

关键词

工频磁场黏着斑细胞迁移表皮生长因子受体黏着斑激酶桩蛋白

Keywords

Power frequency magnetic field (PFMF)Focal adhesionCell migrationEpidermal growth factor receptor (EGFR)Focal adhesion kinase (FAK)Paxillin

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