Oncotarget

Research Papers: Pathology:

Porcine reproductive and respiratory syndrome virus triggers mitochondrial fission and mitophagy to attenuate apoptosis

Shuaifeng Li, Jiaxing Wang, Ao Zhou, Faheem Ahmed Khan, Lin Hu and Shujun Zhang _

PDF  |  HTML  |  How to cite  |  Order a Reprint

Oncotarget. 2016; 7:56002-56012. https://doi.org/10.18632/oncotarget.10817

Metrics: PDF 1568 views  |   HTML 1646 views  |   ?  


Abstract

Shuaifeng Li1, Jiaxing Wang1, Ao Zhou1, Faheem Ahmed Khan1, Lin Hu1 and Shujun Zhang1

1 Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan, China

Correspondence to:

Shujun Zhang, email:

Keywords: PRRSV; mitochondrial fission; mitophagy; apoptosis; Pathology Section

Received: January 30, 2016 Accepted: July 09, 2016 Published: July 24, 2016

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) causes acute mitochondrial dysfunction by elevating the level of reactive oxygen species. Mitochondrial dynamics and mitophagy are essential for the maintenance of mitochondrial homeostasis. Here we show that PRRSV infection stimulated mitochondrial fission and mitophagy to attenuate apoptosis in Marc145 cells. PRRSV infection induced the expression of Drp1, enhanced phosphorylation of Drp1 at Ser616 and its subsequent translocation to mitochondria. Furthermore, PRRSV infection increased the expression of PINK1 and Parkin and also stimulated the recruitment of Parkin to mitochondria. In addition, a sensitive dual fluorescence vector expressing mito-mRFP-EGFP targeted mitochondria was employed to observe the complete mitophagy by delivering dysfunctional mitochondria to lysosome for degradation. Interfering the expression of Drp1 and or Parkin suppressed PRRSV replication. More importantly, silencing of Drp1 or Parkin caused significant elevation in apoptotic signaling. These results suggest that PRRSV infection stimulates mitochondrial fission and mitophagy to facilitate virus replication most probably by attenuating apoptosis.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 10817