Department of Neurology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
FEBS Open Bio. 2020 Sep;10(9):1758-1764. doi: 10.1002/2211-5463.12923. Epub 2020 Jul 30.
Ferroptosis, a form of iron-dependent cell death caused by lipid peroxidation, has been implicated in neurological and other disorders. However, the mechanism of ferroptosis in oligodendrocytes is unclear. We tested the susceptibility of MO3.13 cells, an oligodendrocyte line, to ferroptosis after erastin treatment. Immature MO3.13 cells were more susceptible to erastin-induced ferroptosis than chemically differentiated mature MO3.13 cells. Increased expression of solute carrier family 7 member 11 (SLC7A11), which encodes a cystine/glutamate transporter, and greater glutathione concentrations were observed in mature compared with immature MO3.13 cells, linking glutathione to the resistance of mature MO3.13 cells to erastin-induced ferroptosis. These findings highlight the usefulness of immature MO3.13 cells in studies of ferroptosis and investigations into neuropathologies that involve oligodendrocytes.
铁死亡是一种由脂质过氧化引起的铁依赖性细胞死亡形式,与神经和其他疾病有关。然而,少突胶质细胞中铁死亡的机制尚不清楚。我们在 erastin 处理后测试了少突胶质细胞系 MO3.13 细胞对铁死亡的敏感性。未成熟的 MO3.13 细胞比化学分化的成熟 MO3.13 细胞更容易受到 erastin 诱导的铁死亡。在成熟的 MO3.13 细胞中观察到溶质载体家族 7 成员 11(SLC7A11)的表达增加,其编码半胱氨酸/谷氨酸转运体,并且谷胱甘肽浓度更高,将谷胱甘肽与成熟 MO3.13 细胞对 erastin 诱导的铁死亡的抗性联系起来。这些发现突出了不成熟 MO3.13 细胞在铁死亡研究以及涉及少突胶质细胞的神经病理学研究中的有用性。