Ecdysone induction of MsrA protects against oxidative stress in Drosophila
Ecdysone induction of MsrA protects against oxidative stress in Drosophila
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DOI：
10.1016/j.bbrc.2007.01.005
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发表时间：
2007-03-09
影响因子：
3.1
通讯作者：
Weissbach, H.
中科院分区：
文献类型：
--
作者：
Roesijadi, G.;Rezvankhah, S.;Weissbach, H.
甲硫氨酸亚砜还原酶 MsrA 和 MsrB 以差向异构体特异性方式将 Met(O) 还原为 Met。在果蝇中，主要的蜕皮激素诱导蛋白是 MsrA，它受到 EcR-USP 复合物的调节。我们测试了 Kc 细胞对蜕皮激素对 MsrA、MsrB、EcR 和 CA T 的诱导，发现 MsrA 和 EcR 受蜕皮激素诱导，但 MsrB 和 CA T 则不然。当我们测试对 20 mM H2O2 毒性的抵抗力时，Kc 细胞的活力降低了 3 倍。在接触 H2O2 之前用 0.2 μM 蜕皮激素预处理 48 小时。对照的存活率提高至 77%。 EcR缺陷的L57-3-11敲除系对蜕皮激素没有反应，并且对照和经蜕皮激素处理的L57-3-11细胞的H2O2抗性与未经蜕皮激素处理的Kc细胞相似。这些结果表明，MsrA 的激素调节与果蝇模型中针对氧化应激的保护有关。 (c) 2007 Elsevier Inc. 保留所有权利。
The methionine sulfoxide reductases MsrA and MsrB reduce Met(O) to Met in epimer-specific fashion. In Drosophila, the major ecdysone induced protein is MsrA, which is regulated by the EcR-USP complex. We tested Kc cells for induction of MsrA, MsrB, EcR, and CA T by ecdysone and found that MsrA and the EcR were induced by ecdysone, but MsrB and CA T were not. When we tested for resistance to 20 mM H2O2 toxicity, viability of Kc cells was reduced 3-fold. Pretreatment with 0.2 mu M ecdysone for 48 h prior to exposure to H2O2. increased viability to 77% of controls. The EcR-deficient L57-3-11 knockout line was not responsive to ecdysone, and H2O2 resistance of both control and ecdysone-treated L57-3-11 cells was similar to that of the ecdysone-untreated Kc cells. These results show that hormonal regulation of MsrA is implicated in conferring protection against oxidative stress in the Drosophila model. (c) 2007 Elsevier Inc. All rights reserved.