TY - JOUR
T1 - Caspase-3 activation and ERK phosphorylation during CVB3 infection of cells
T2 - Influence of the coxsackievirus and adenovirus receptor and engineered variants
AU - Cunningham, Kelly A.
AU - Chapman, Nora M.
AU - Carson, Steven D.
N1 - Funding Information:
A College of Medicine Research Grant Award supported this work. Kelly Cunningham was partially supported by the Department of Medical and Health Sciences, University of Newcastle, Australia, and the Hunter Medical Research Institute. This work was completed while Kelly Cunningham was a doctoral student in the laboratory of Dr Darren R. Shafren, University of Newcastle, and she gratefully acknowledges his support. Justin Hobbs provided valuable assistance with this work.
PY - 2003/4/1
Y1 - 2003/4/1
N2 - Caspase activation and MAP kinase signaling have been implicated in coxsackievirus B3 (CVB3) pathogenesis, and both have been demonstrated late in the virus life cycle. We studied activation of caspase-3, an effector protease of apoptosis, and ERK phosphorylation, indicative of MAPK signaling pathway activation, following CVB3 infection of cells that express the coxsackievirus and adenovirus receptor (CAR) or CAR constructs lacking the cytoplasmic domain, and cells which express no detectable CAR. These experiments showed that a burst of caspase-3 activity preceded lysis of CVB3-infected cells expressing CAR, irrespective of the CAR cytoplasmic domain. In RD cells, which were infected in the absence of detectable CAR, caspase-3 activity increased progressively over 52 h with no apparent burst. ERK phosphorylation also occurred late in the virus life cycle, preceding caspase-3 activation, and occurred in cells expressing full-length CAR but not in RD. These results show that ERK phosphorylation precedes caspase-3 activation, both occur late in the infection, and both are influenced by the presence of CAR.
AB - Caspase activation and MAP kinase signaling have been implicated in coxsackievirus B3 (CVB3) pathogenesis, and both have been demonstrated late in the virus life cycle. We studied activation of caspase-3, an effector protease of apoptosis, and ERK phosphorylation, indicative of MAPK signaling pathway activation, following CVB3 infection of cells that express the coxsackievirus and adenovirus receptor (CAR) or CAR constructs lacking the cytoplasmic domain, and cells which express no detectable CAR. These experiments showed that a burst of caspase-3 activity preceded lysis of CVB3-infected cells expressing CAR, irrespective of the CAR cytoplasmic domain. In RD cells, which were infected in the absence of detectable CAR, caspase-3 activity increased progressively over 52 h with no apparent burst. ERK phosphorylation also occurred late in the virus life cycle, preceding caspase-3 activation, and occurred in cells expressing full-length CAR but not in RD. These results show that ERK phosphorylation precedes caspase-3 activation, both occur late in the infection, and both are influenced by the presence of CAR.
KW - Apoptosis
KW - Caspase-3
KW - Coxsackievirus
KW - MAP kinase
KW - Receptor
UR - http://www.scopus.com/inward/record.url?scp=0347926114&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0347926114&partnerID=8YFLogxK
U2 - 10.1016/S0168-1702(03)00044-3
DO - 10.1016/S0168-1702(03)00044-3
M3 - Article
C2 - 12686427
AN - SCOPUS:0347926114
VL - 92
SP - 179
EP - 186
JO - Virus Research
JF - Virus Research
SN - 0168-1702
IS - 2
ER -