|ZFIN ID: ZDB-PUB-080306-1|
Zebrafish anti-apoptotic protein zfBcl-x(L) can block betanodavirus protein alpha-induced mitochondria-mediated secondary necrosis cell death
Wu, H.C., Chiu, C.S., Wu, J.L., Gong, H.Y., Chen, M.C., Lu, M.W., and Hong, J.R.
|Source:||Fish & shellfish immunology 24(4): 436-449 (Journal)|
|Registered Authors:||Gong, Hong-Yi, Hong, Jiann-Ruey, Wu, Jen-Leih|
|Keywords:||Nervous necrosis virus, Protein α, Mitochondria, zfBcl-xL, Apoptosis, Secondary necrosis cell death|
|PubMed:||18276161 Full text @ Fish Shellfish Immunol.|
Wu, H.C., Chiu, C.S., Wu, J.L., Gong, H.Y., Chen, M.C., Lu, M.W., and Hong, J.R. (2008) Zebrafish anti-apoptotic protein zfBcl-x(L) can block betanodavirus protein alpha-induced mitochondria-mediated secondary necrosis cell death. Fish & shellfish immunology. 24(4):436-449.
ABSTRACTBetanodavirus protein alpha induces cell apoptosis or secondary necrosis by a poorly understood process. In the present work, red spotted grouper nervous necrosis virus (RGNNV) RNA 2 was cloned and transfected into tissue culture cells (GF-1) which then underwent apoptosis or post-apoptotic necrosis. In the early apoptotic stage, progressive phosphatidylserine externalization was evident at 24h post-transfection (p.t.) by Annexin V-FLUOS staining. TUNEL assay revealed apoptotic cells at 24-72h p.t, after which post-apoptotic necrotic cells were identified by acridine orange/ethidium bromide dual dye staining from 48 to 72h p.t. Protein alpha induced progressive loss of mitochondrial membrane potential (MMP) which was detected in RNA2-transfected GF-1 cells at 24, 48, and 72h p.t., which correlated with cytochrome c release, especially at 72h p.t. To assess the effect of zfBcl-x(L) on cell death, RNA2-transfected cells were co-transfected with zfBcl-x(L). Co-transfection of GF-1 cells prevented loss of MMP at 24h and 48h p.t. and blocked initiator caspase-8 and effector caspase-3 activation at 48h p.t. We conclude that RGNNV protein alpha induces apoptosis followed by secondary necrotic cell death through a mitochondria-mediated death pathway and activation of caspases-8 and -3.
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