Essler Silke, Dehne Nathalie, Brüne Bernhard
Goethe-University Frankfurt, Faculty of Medicine, Biochemistry I, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
FEBS Lett. 2009 Nov 3;583(21):3531-5. doi: 10.1016/j.febslet.2009.10.017. Epub 2009 Oct 12.
Reactive oxygen species not only serve as signaling molecules, they also contribute to oxidative stress and cell damage. The thioredoxin and glutaredoxin systems form along with peroxiredoxins a precisely regulated defense system to maintain the cellular redox homeostasis. There is evidence that nitric oxide (NO) protects cells from oxidative stress by preventing inactivation of peroxiredoxins by sulfinylation. Here we demonstrate that NO and hypoxia upregulate Sestrin2 by HIF-1-dependent and additional mechanisms and that Sestrin2 contributes to preventing peroxiredoxins from sulfinylation. We conclude that Sestrin2 plays a role in peroxide defense as a reductase for peroxiredoxins.
活性氧不仅作为信号分子，还会导致氧化应激和细胞损伤。硫氧还蛋白和谷氧还蛋白系统与过氧化物酶一起形成了一个精确调控的防御系统，以维持细胞的氧化还原稳态。有证据表明，一氧化氮（NO）通过防止过氧化物酶被亚磺酰化失活来保护细胞免受氧化应激。在此，我们证明NO和缺氧通过HIF-1依赖及其他机制上调Sestrin2，且Sestrin2有助于防止过氧化物酶被亚磺酰化。我们得出结论，Sestrin2作为过氧化物酶的还原酶在过氧化物防御中发挥作用。
