Overexpression of pig selenoprotein S blocks OTA-induced promotion of PCV2 replication by inhibiting oxidative stress and p38 phosphorylation in PK15 cells.
Overexpression of pig selenoprotein S blocks OTA-induced promotion of PCV2 replication by inhibiting oxidative stress and p38 phosphorylation in PK15 cells.
复制标题
猪硒蛋白 S 的过表达通过抑制 PK15 细胞中的氧化应激和 p38 磷酸化来阻断 OTA 诱导的 PCV2 复制促进。
DOI：
10.18632/oncotarget.7814
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发表时间：
2016-04-12
期刊：
影响因子：
--
通讯作者：
Huang K
中科院分区：
文献类型：
--
作者：
Gan F;Hu Z;Huang Y;Xue H;Huang D;Qian G;Hu J;Chen X;Wang T;Huang K
猪圆环病毒2型（PCV2）是猪圆环病毒病的主要病因，赭曲霉毒素A （OTA）诱导的氧化应激促进了PCV2的复制。在人类中，硒蛋白S （seloprotein S, SelS）具有抗氧化能力，但SelS是否影响病毒感染尚不清楚。在这里，我们用猪pCDNA3.1-SelS稳定转染PK15细胞以过表达SelS。2 μM或4 μM硒（Se）和SelS过表达可阻断ota诱导的PCV2 DNA拷贝数和感染细胞数的增加。过表达SelS还会增加谷胱甘肽（GSH）、nf - e2相关因子2 (Nrf2) mRNA和γ-谷氨酰半胱氨酸合成酶mRNA水平；活性氧（ROS）水平降低；并且在pcv2感染的PK15细胞中抑制p38磷酸化，无论OTA治疗如何。丁硫氨酸亚砜可逆转上述sels诱导的变化。在经ta处理的PK15细胞中，sirna介导的SelS敲低可降低Nrf2 mRNA和GSH水平，增加ROS水平，促进PCV2复制。这些数据表明，猪SelS通过抑制PK15细胞的氧化应激和p38磷酸化来阻断ota诱导的PCV2复制。
Porcine circovirus type 2 (PCV2) is the primary cause of porcine circovirus disease, and ochratoxin A (OTA)-induced oxidative stress promotes PCV2 replication. In humans, selenoprotein S (SelS) has antioxidant ability, but it is unclear whether SelS affects viral infection. Here, we stably transfected PK15 cells with pig pCDNA3.1-SelS to overexpress SelS. Selenium (Se) at 2 or 4 μM and SelS overexpression blocked the OTA-induced increases of PCV2 DNA copy number and infected cell numbers. SelS overexpression also increased glutathione (GSH), NF-E2-related factor 2 (Nrf2) mRNA, and γ-glutamyl-cysteine synthetase mRNA levels; decreased reactive oxygen species (ROS) levels; and inhibited p38 phosphorylation in PCV2-infected PK15 cells, regardless of OTA treatment. Buthionine sulfoximine reversed all of the above SelS-induced changes. siRNA-mediated SelS knockdown decreased Nrf2 mRNA and GSH levels, increased ROS levels, and promoted PCV2 replication in OTA-treated PK15 cells. These data indicate that pig SelS blocks OTA-induced promotion of PCV2 replication by inhibiting the oxidative stress and p38 phosphorylation in PK15 cells.