线粒体生成的活性氧对 RGK1 细胞中 Nrf2/Keap1 信号通路的调节作用。
Evidence of Nrf2/Keap1 Signaling Regulation by Mitochodria-Generated Reactive Oxygen Species in RGK1 Cells.
机构信息
Department of Oncology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8544, Japan.
Amanogawa Galactic Astronomy Research Center (AGARC), Graduate School of Sciences, Kagoshima University, Kagoshima 890-0065, Japan.
出版信息
Biomolecules. 2023 Feb 27;13(3):445. doi: 10.3390/biom13030445.
It has been known that reactive oxygen species (ROS) are generated from the mitochondrial electron transport chain (ETC). Majima et al. proved that mitochondrial ROS (mtROS) caused apoptosis for the first time in 1998 (Majima et al. J Biol Chem, 1998). It is speculated that mtROS can move out of the mitochondria and initiate cellular signals in the nucleus. This paper aims to prove this phenomenon by assessing the change in the amount of manganese superoxide dismutase (MnSOD) by MnSOD transfection. Two cell lines of the same genetic background, of which generation of mtROS are different, i.e., the mtROS are more produced in RGK1, than in that of RGM1, were compared to analyze the cellular signals. The results of immunocytochemistry staining showed increase of Nrf2, Keap1, HO-1 and 2, MnSOD, GCL, GST, NQO1, GATA1, GATA3, GATA4, and GATA5 in RGK1 compared to those in RGM1. Transfection of human MnSOD in RGK1 cells showed a decrease of those signal proteins, suggesting mtROS play a role in cellular signals in nucleus.
已知活性氧（ROS）是由线粒体电子传递链（ETC）产生的。1998 年，Majima 等人首次证明线粒体 ROS（mtROS）导致细胞凋亡（Majima 等人，《生物化学杂志》，1998 年）。据推测，mtROS 可以从线粒体中逸出，并在细胞核中引发细胞信号。本文旨在通过评估 MnSOD 转染引起的锰超氧化物歧化酶（MnSOD）量的变化来证明这一现象。比较了两种遗传背景相同的细胞系，即 RGK1 比 RGM1 产生更多的 mtROS，以分析细胞信号。免疫细胞化学染色结果显示，与 RGM1 相比，RGK1 中的 Nrf2、Keap1、HO-1 和 2、MnSOD、GCL、GST、NQO1、GATA1、GATA3、GATA4 和 GATA5 的表达增加。在 RGK1 细胞中转染人 MnSOD 可降低这些信号蛋白的表达，表明 mtROS 在细胞核中的细胞信号中发挥作用。
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