Overexpression of pig selenoprotein S blocks OTA-induced promotion of PCV2 replication by inhibiting oxidative stress and p38 phosphorylation in PK15 cells
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Fang Gan1,2, Zhihua Hu1,2, Yu Huang1,2, Hongxia Xue1,2, Da Huang1,2, Gang Qian1,2, Junfa Hu1,2, Xingxiang Chen1,2, Tian Wang3, Kehe Huang1,2
1College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, Jiangsu Province, China
2Institute of Nutritional and Metabolic Disorders in Domestic Animals and Fowls, Nanjing Agricultural University, Nanjing 210095, Jiangsu Province, China
3College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, Jiangsu Province, China
Kehe Huang, e-mail: [email protected]
Tian Wang, e-mail: [email protected]
Keywords: overexpression of selenoprotein S, ochratoxin A, porcine circovirus type 2, oxidative stress, p38 signaling pathway
Received: November 16, 2015 Accepted: February 20, 2016 Published: March 01, 2016
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.
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