铜诱导的小鼠肾毒性通过调节 Atox1 受 period1 控制。

IF 1.3 4区 医学 Q4 MEDICINE, RESEARCH & EXPERIMENTAL
Sarah Tominaga, Hiroki Yoshioka, Satoshi Yokota, Yosuke Tsukiboshi, Masumi Suzui, Makoto Nagai, Hirokazu Hara, Nobuhiko Miura, Tohru Maeda
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引用次数: 0

摘要

众所周知,铜(Cu)可诱导肝脏、肾脏和大脑中的氧化应激和细胞凋亡。我们之前证明了铜诱导肝脏昼夜变化的分子机制。然而,参与铜诱导肾脏慢性毒性的细胞分子仍然未知。在本研究中,我们旨在阐明铜诱导肾脏昼夜毒性的分子机制。我们评估了铜处理后小鼠肾皮质肾小管细胞(MuRTE61 细胞)的细胞活力和时钟基因表达水平。我们还检测了MuRTE61细胞过表达周期1(Per1)后的铜平衡和凋亡相关基因水平。Cu处理以剂量依赖的方式降低了MuRTE61细胞的活力。值得注意的是,Per1 的过表达缓解了 Cu 诱导的对 MuRTE61 细胞活力的抑制。此外,Per1 的过表达下调了已裂解的 caspase-3,并通过上调抗氧化剂 1 铜伴侣(Atox1)的水平降低了铜的水平。这些结果表明,铜诱导的肾毒性与 Per1 通过调节铜伴侣 Atox1 的表达有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Copper-induced renal toxicity controlled by period1 through modulation of Atox1 in mice.

Copper (Cu) is known to induce oxidative stress and apoptosis in the liver, kidney, and brain. We previously demonstrated the molecular mechanism underlying the Cu-induced hepatic diurnal variation. However, the cellular molecule(s) involved in Cu-induced renal chronotoxicity remain unknown. In this study, we aimed to elucidate the molecular mechanisms underlying Cu-induced diurnal toxicity in the kidneys. We evaluated cell viability and clock gene expression levels in mouse renal cortex tubular cells (MuRTE61 cells) after Cu treatment. We also examined the Cu homeostasis- and apoptosis-related gene levels after period 1 (Per1) overexpression in MuRTE61 cells. Cu treatment decreased MuRTE61 cell viability in a dose-dependent manner. It increased the Per1 expression levels after 24 h. Notably, Per1 overexpression alleviated the Cu-induced inhibition of MuRTE61 cell viability. Moreover, Per1 overexpression downregulated the cleaved caspase-3 and reduced Cu levels by upregulating the antioxidant 1 copper chaperone (Atox1) levels. These results suggest that Cu-induced renal toxicity is associated with Per1 expression via the regulation of the copper chaperone, Atox1.

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来源期刊
Biomedical Research-tokyo
Biomedical Research-tokyo 医学-医学:研究与实验
CiteScore
2.40
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Biomedical Research is peer-reviewed International Research Journal . It was first launched in 1990 as a biannual English Journal and later became triannual. From 2008 it is published in Jan-Apr/ May-Aug/ Sep-Dec..
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