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.

中文翻译：

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在人类少突胶质细胞系的成熟过程中，对erastin 诱导的铁死亡的易感性降低。

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，与神经系统和其他疾病有关。然而，少突胶质细胞铁死亡的机制尚不清楚。我们测试了 MO3.13 细胞（一种少突胶质细胞系）对erastin 治疗后铁死亡的敏感性。与化学分化的成熟 MO3.13 细胞相比，未成熟的 MO3.13 细胞更容易受到erastin 诱导的铁死亡。编码胱氨酸/谷氨酸转运蛋白的溶质载体家族 7 成员 11 (SLC7A11) 的表达增加，与未成熟的 MO3.13 细胞相比，在成熟细胞中观察到更高的谷胱甘肽浓度，这将谷胱甘肽与成熟 MO3.13 细胞对erastin 的抗性联系起来诱导的铁死亡。这些发现突出了未成熟 MO3 的有用性。