This Journal is indexed and abstracted in
Kafkas Üniversitesi Veteriner Fakültesi Dergisi 2017 , Vol 23 , Issue 4
Lentivirus-mediated bta-miR-193a Overexpression Promotes Apoptosis of MDBK Cells by Targeting BAX and Inhibits BVDV Replication
HU N1, FU Q2, HU S3, SHI M4, SHI H2, NI W3, SHENG J1, CHEN C1
1College of Animal Science and Technology, Shihezi University, Shihezi 832003, Xinjiang, CHINA
2College of Veterinary Medicine, Xinjiang Agricultural University, Urumqi 830052, Xinjiang, CHINA
3College of Life Technology, Shihezi University, Shihezi 832003, Xinjiang, CHINA
4No. 2 Middle School of Shihezi, Shihezi 832000, Xinjiang, CHINA
DOI : 10.9775/kvfd.2017.17428 MicroRNAs (miRNAs) are a class of naturally occurring, short, endogenous, noncoding RNA molecules (~22 nt) involved in a wide variety of regulatory pathways, including cell growth, development, differentiation, proliferation, and apoptosis, as well as viral defense, hematopoiesis, organ formation, and metabolism. Previous studies showed that bta-miR-193a (miR-193a) was upregulated in Madin-Darby bovine kidney (MDBK) cells infected with bovine viral diarrhea virus (BVDV) strain NADL; however, the role of miR-193a in apoptosis-associated regulation remains unclear. In this study, we found that miR-193a is a novel regulator of MDBK apoptosis and that lentiviral infection exhibited a positive effect on miR-193a expression. Additionally, we observed that the miR-193a-target sequence was present in the 3′-untranslated region of B-cell lymphoma-2-associated X protein (BAX) mRNA, with miR-193a overexpression resulting in reduced BAX mRNA and protein levels. Furthermore, we observed that miR-193a promoted apoptosis and inhibited BVDV strain NADL replication according to quantitative reverse transcription polymerase chain reaction results. These findings confirmed miR-193a as a positive regulator of apoptosis and provided a theoretical basis for the important role of miRNAs in regulating BVDV replication. Keywords : Lentivirus, miR-193a, Apoptosis, BAX, BVDV strain NADL