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Regulation of ROS in transmissible gastroenteritis virus-activated apoptotic signaling.

Abstract：

:Transmissible gastroenteritis virus (TGEV), an enteropathogenic coronavirus, causes severe lethal watery diarrhea and dehydration in piglets. Previous studies indicate that TGEV infection induces cell apoptosis in host cells. In this study, we investigated the roles and regulation of reactive oxygen species (ROS) in TGEV-activated apoptotic signaling. The results showed that TGEV infection induced ROS accumulation, whereas UV-irradiated TGEV did not promote ROS accumulation. In addition, TGEV infection lowered mitochondrial transmembrane potential in PK-15 cell line, which could be inhibited by ROS scavengers, pyrrolidinedithiocarbamic (PDTC) and N-acetyl-l-cysteine (NAC). Furthermore, the two scavengers significantly inhibited the activation of p38 MAPK and p53 and further blocked apoptosis occurrence through suppressing the TGEV-induced Bcl-2 reduction, Bax redistribution, cytochrome c release and caspase-3 activation. These results suggest that oxidative stress pathway might be a key element in TGEV-induced apoptosis and TGEV pathogenesis.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Ding L,Zhao X,Huang Y,Du Q,Dong F,Zhang H,Song X,Zhang W,Tong D

doi

10.1016/j.bbrc.2013.10.164

subject

Has Abstract

pub_date

2013-12-06 00:00:00

pages

33-7

issue

1-2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(13)01866-4

journal_volume

442

pub_type

杂志文章

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