TY - JOUR
T1 - Infectious pancreatic necrosis virus induces apoptosis due to down-regulation of survival factor MCL-1 protein expression in a fish cell line
AU - Hong, Jiann Ruey
AU - Hsu, Ya Li
AU - Wu, Jen Leih
N1 - Funding Information:
We thank Dr Dauglas Platt for reviewing this manuscript and providing helpful comments. This work was supported by grants awarded to J.-L.W. from the National Science Council, Republic of China.
PY - 1999/9
Y1 - 1999/9
N2 - Infectious pancreatic necrosis virus (IPNV), a member of the virus family Birnaviridae, causes an acute, contagious disease in a number of economically important fish species. CHSE-214, a Chinook salmon embryonic cell line, when infected by IPNV showed morphological and biochemical features of apoptosis, including an intense DNA laddering pattern and blebbing of the plasma membrane, followed by formation of apoptotic bodies. The Mcl-1 gene product proved to be a member of the Bcl-2 gene family, and like Bcl-2 had the capacity to promote cell viability. Here, we investigated the pattern of expression of Mcl-1 in CHSE-214 cells infected by IPNV. We found that the Mcl-1 level decreased markedly in cells undergoing apoptosis after IPNV infection. This decrease was rapid during the first 8 h postinfection and preceded cell death. Furthermore, we found that drugs including cycloheximide, genistein and EDTA either prevented the decline in Mcl-1 levels or blocked the intense DNA laddering pattern. Other drugs like serine proteinase inhibitor, 400 μg/ml aprotinin, 400 μg/ml leupeptin and 100 μg/ml tryphostin did not. The virus gene expression pattern was examined by Western blot using antivirion polyclonal antibody and was blocked during treatment with cycloheximide, genistein and EDTA but not by serine proteinase, aprotinin, leupeptin or tryphostin. Together the data showed a striking correlation between virus replication and Mcl-1 expression in CHSE-214 cells, suggesting that the virus gene expression has a possible involvement with Mcl-1 in the regulation of apoptosis in these cells. Copyright (C) 1999 Elsevier Science B.V.
AB - Infectious pancreatic necrosis virus (IPNV), a member of the virus family Birnaviridae, causes an acute, contagious disease in a number of economically important fish species. CHSE-214, a Chinook salmon embryonic cell line, when infected by IPNV showed morphological and biochemical features of apoptosis, including an intense DNA laddering pattern and blebbing of the plasma membrane, followed by formation of apoptotic bodies. The Mcl-1 gene product proved to be a member of the Bcl-2 gene family, and like Bcl-2 had the capacity to promote cell viability. Here, we investigated the pattern of expression of Mcl-1 in CHSE-214 cells infected by IPNV. We found that the Mcl-1 level decreased markedly in cells undergoing apoptosis after IPNV infection. This decrease was rapid during the first 8 h postinfection and preceded cell death. Furthermore, we found that drugs including cycloheximide, genistein and EDTA either prevented the decline in Mcl-1 levels or blocked the intense DNA laddering pattern. Other drugs like serine proteinase inhibitor, 400 μg/ml aprotinin, 400 μg/ml leupeptin and 100 μg/ml tryphostin did not. The virus gene expression pattern was examined by Western blot using antivirion polyclonal antibody and was blocked during treatment with cycloheximide, genistein and EDTA but not by serine proteinase, aprotinin, leupeptin or tryphostin. Together the data showed a striking correlation between virus replication and Mcl-1 expression in CHSE-214 cells, suggesting that the virus gene expression has a possible involvement with Mcl-1 in the regulation of apoptosis in these cells. Copyright (C) 1999 Elsevier Science B.V.
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U2 - 10.1016/S0168-1702(99)00060-X
DO - 10.1016/S0168-1702(99)00060-X
M3 - Article
C2 - 10509718
AN - SCOPUS:0032855027
SN - 0168-1702
VL - 63
SP - 75
EP - 83
JO - Virus Research
JF - Virus Research
IS - 1-2
ER -