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首页> 外文期刊>Cell cycle >The induction of thioredoxin-1 by epinephrine withdraws stress via interaction with beta-arrestin-1
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The induction of thioredoxin-1 by epinephrine withdraws stress via interaction with beta-arrestin-1

机译：肾上腺素对硫氧还蛋白-1的诱导通过与β-arrestin-1的相互作用减轻压力

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Stress regulates a panel of important physiological functions and disease states. Epinephrine is produced under stresses threaten to homeostasis. Thioredoxin-1(Trx-1) is a redox regulating protein which is induced to resist stresses and related with various diseases. Thus, it is important to examine whether Trx-1 is induced by epinephrine and to understand the underlying molecular mechanisms that Trx-1 modulates epinephrine stress. Here, we show that the expression of Trx-1 was induced by epinephrine via -adrenergic receptor/Cyclic AMP/protein kinase A (PKA) signaling pathway in PC12 cells. The down-regulation of Trx-1 by siRNA aggravated accumulation of -H2AX and further decreased expression of p53 by epinephrine. Accordingly, Trx-1 overexpression alleviated accumulation of -H2AX and restored the expressions of p53 and C/EBP homologous protein (CHOP) in the cortex, hippocampus and thymus of mice. Moreover, Trx-1 overexpression reduced the malondialdehyde concentration by epinephrine. We further explored the mechanism on p53 and -H2AX regulated by Trx-1. We found that overexpression of Trx-1 suppressed -arrestin-1 expression through interaction with -arrestin-1. Consequently, the downregulation of -arrestin-1 suppressed the cell viability and the expressions of -H2AX and cyclin D1, and increased p53 expression. Taken together, our data suggest that Trx-1/-arrestin-1 interaction may represent a novel endogenous mechanism on protecting against stress.
机译：压力调节着重要的生理功能和疾病状态。肾上腺素是在对体内稳态有威胁的压力下产生的。硫氧还蛋白-1（Trx-1）是一种氧化还原调节蛋白，被诱导抵抗压力并与多种疾病有关。因此，重要的是要检查Trx-1是否被肾上腺素诱导，并了解Trx-1调节肾上腺素应激的潜在分子机制。在这里，我们显示肾上腺素通过-肾上腺素受体/循环AMP /蛋白激酶A（PKA）信号通路诱导肾上腺素Trx-1的表达。 siRNA对Trx-1的下调加重了-H2AX的积累，肾上腺素进一步降低了p53的表达。因此，Trx-1的过表达减轻了-H2AX的积累，并恢复了小鼠皮层，海马和胸腺中p53和C / EBP同源蛋白（CHOP）的表达。此外，Trx-1的过表达降低了肾上腺素引起的丙二醛浓度。我们进一步探讨了Trx-1调控p53和-H2AX的机制。我们发现Trx-1的过表达通过与-arrestin-1相互作用抑制-arrestin-1的表达。因此，-arrestin-1的下调抑制了细胞活力以及-H2AX和细胞周期蛋白D1的表达，并增加了p53的表达。两者合计，我们的数据表明，Trx-1 / -arrestin-1相互作用可能代表了一种新型的内源性机制，可预防压力。

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