Essential role of thioredoxin 2 in mitigating oxidative stress in retinal epithelial cells.
Essential role of thioredoxin 2 in mitigating oxidative stress in retinal epithelial cells.
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DOI：
10.1155/2013/185825
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发表时间：
2013
影响因子：
1.9
通讯作者：
Tomita H
中科院分区：
文献类型：
--
作者：
Sugano E;Murayama N;Takahashi M;Tabata K;Tamai M;Tomita H
视网膜不断受到氧化应激，这是由视网膜色素上皮（RPE）细胞中存在的有效的抗氧化系统抵消。这些系统的破坏导致年龄相关性黄斑变性的发展。硫氧还蛋白2（Trx 2）是一种有效的抗氧化剂，其直接作用于线粒体。在本研究中，使用4-羟基壬烯醛（4-HNE）或C2-神经酰胺在人RPE细胞系（ARPE-19）中诱导氧化应激。通过评估细胞活力、细胞死亡动力学、线粒体代谢活性和热休克蛋白（Hsps）在Trx 2过表达细胞系中的表达来研究Trx 2对氧化应激的保护作用，所述Trx 2过表达细胞系通过用编码Trx 2的腺相关病毒载体转染ARPE细胞产生。我们发现，Trx 2的过度表达减少了这两种药物诱导的细胞死亡时，他们在低浓度存在。此外，在诱导氧化应激后早期，Trx 2通过上调线粒体代谢活性和抑制Hsp 70表达在维持细胞活力中起关键作用。
The retina is constantly subjected to oxidative stress, which is countered by potent antioxidative systems present in retinal pigment epithelial (RPE) cells. Disruption of these systems leads to the development of age-related macular degeneration. Thioredoxin 2 (Trx2) is a potent antioxidant, which acts directly on mitochondria. In the present study, oxidative stress was induced in the human RPE cell line (ARPE-19) using 4-hydroxynonenal (4-HNE) or C2-ceramide. The protective effect of Trx2 against oxidative stress was investigated by assessing cell viability, the kinetics of cell death, mitochondrial metabolic activity, and expression of heat shock proteins (Hsps) in Trx2-overexpressing cell lines generated by transfecting ARPE cells with an adeno-associated virus vector encoding Trx2. We show that overexpression of Trx2 reduced cell death induced by both agents when they were present in low concentrations. Moreover, early after the induction of oxidative stress Trx2 played a key role in the maintenance of the cell viability through upregulation of mitochondrial metabolic activity and inhibition of Hsp70 expression.
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DOI：
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