この研究は、50 Hz, 100 μTの磁界がNB69ヒト神経芽腫細胞株の増殖を引き起こすか否か、またこの増殖にMAPK-ERK1/2 （Mitogen-Activated Protein Kinase - Extracellular-Signal-Regulated Kinase 1 and 2）シグナリング経路が関与するか否かを調べた。培養開始4日目から細胞に磁界ばく露を与えた。ヘルムホルツコイルによる均一磁界へのばく露を63時間、断続的（5分間ON／10分間OFFまたは3時間ON／3時間OFFの2通り）または連続的に行った。擬似ばく露、断続ばく露、連続ばく露は全てブラインドで行った。その結果、連続ばく露では細胞増殖の有意な変化はなかった；断続ばく露では、S期の細胞の割合が統計的に有意に増加し、結果として細胞数が有意に増加した；断続ばく露では、早期の一過性・反復性のERK1/2活性化も誘導されていた；この増殖反応およびERK1/2活性化はMEK (ERK kinases 1 and 2)の特異的阻害剤により阻止されることが確認された、などの所見を報告している。
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To study whether a 50 Hz magnetic field can induce cell proliferation in the human neuroblastoma cell line NB69, and whether the signaling pathway MAPK-ERK1/2 is involved in that proliferative response.
The possible involvement of the transcription factor CREB in the proliferative response to the magnetic field was also investigated.
|ばく露装置の詳細||two pairs of Helmholtz coils set in two magnetically shielded conetic alloy chambers which were placed inside two identical CO2 incubators; cells in Petri dishes placed in the center of the coil system; only one set of coils was energized (samples in the unenergized set were considered as sham-exposed controls)|
|Sham exposure||A sham exposure was conducted.|
The continuous exposure did not induce significant changes in cell proliferation. In contrast, both intermittent exposure to the 50 Hz magnetic field significantly stimulated cell proliferation in NB69 cells. The magnetic field exposure induced repeated transient activation of the MAPK- ERK1/2 signaling pathway, occurring early after the onset of each of the exposure cycles of the intermittent exposure (peak during "on"-interval).
When a specific inhibitor (PD98059) of the MAPK-ERK1/2 pathway was added to the culture medium, the early activation of ERK1/2 and the proliferative response observed subsequently, were blocked. From this, the authors conclude that activation of ERK1/2 is involved in the molecular mechanisms through which the 50 Hz magnetic field induces a proliferative response in NB69 cells. Additionally, the data showed that the magnetic field exposure also activated CREB, a downstream target of the MAPK- ERK1/2 pathway. However, such activation was independent of ERK1/2, suggesting that other pathways could be involved in the cellular and molecular response to the magnetic field.
These findings provide a further insight into the mechanisms through which weak, 50 Hz magnetic field could influence cancer-related processes in human cells.