Abstract：
Schwannomas are benign tumors of the peripheral nervous system arising from the transformation of Schwann cells (SCs). On the whole, these tumors are related to alterations of the neurofibromin type 2 gene, coding for the oncosuppressor merlin, a cytoskeleton-associated protein belonging to the ezrin-radixin-moesin family. However, the underlying mechanisms of schwannoma onset and progression are not fully elucidated, whereas one of the challenges might be the environment. In this light, the exposure to electromagnetic field (EMF), generated by the use of common electrical devices, has been defiantly suggested as the cause of SCs transformation even if the evidence was mostly epidemiologic. Indeed, insubstantial mechanisms have been so far identified to explain SCs oncotransformation. Recently, some in vitro evidence pointed out alterations in proliferation and migration abilities in SCs exposed to EMF (0.1 T, 50 Hz, 10 min). Here, we used the same experimental paradigma to discuss the involvement of putative epigenetic mechanisms in SCs adaptation to EMF and to explain the occurrence of hypoxic alterations after the exposure. Our findings indicate a set of environmental-induced changes in SCs, toward a less-physiological state, which may be pathologically relevant for the SCs differentiation and the schwannoma development.
摘要：
神经鞘瘤是由雪旺氏细胞（SC）的转化引起的周围神经系统的良性肿瘤。总的来说,这些肿瘤与神经纤维蛋白2型基因的改变有关，编码肿瘤抑制因子Merlin,属于ezrin-radixin-moesin家族的细胞骨架相关蛋白。然而,神经鞘瘤发病和进展的潜在机制尚未完全阐明，而其中一个挑战可能是环境。在这种情况下，暴露于电磁场（EMF），使用普通电气设备产生的，即使证据主要是流行病学证据，也被认为是SC转化的原因。的确,到目前为止，已经确定了解释SCs共转化的非实质性机制。最近,一些体外证据指出暴露于EMF的SC的增殖和迁移能力的改变(0.1T，50Hz,10分钟)。这里,我们使用相同的实验范式来讨论假定的表观遗传机制参与SC对EMF的适应,并解释暴露后低氧改变的发生.我们的发现表明一组环境诱导的SCs变化，朝着不太生理的状态，这可能与SCs分化和神经鞘瘤的发展在病理上有关。
