Back to Search Start Over

Lentivirus-mediated bta-mir-193a overexpression promotes apoptosis of mdbk cells by targeting bax and inhibits bvdv replication

Authors :
HU N
FU Q
HU S
SHI M
SHI H
NI W
SHENG J
CHEN C
Source :
Kafkas Universitesi Veteriner Fakültesi Dergisi, Vol 23, Iss 4, Pp 587-593 (2017)
Publication Year :
2017
Publisher :
Kafkas University, Faculty of Veterinary Medicine, 2017.

Abstract

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.

Details

Language :
English
ISSN :
13092251
Volume :
23
Issue :
4
Database :
Directory of Open Access Journals
Journal :
Kafkas Universitesi Veteriner Fakültesi Dergisi
Publication Type :
Academic Journal
Accession number :
edsdoj.4fe8c46c82014de4a92e960aae731571
Document Type :
article
Full Text :
https://doi.org/10.9775/kvfd.2017.17428