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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/26848

Title: Zebrafish anti-apoptotic protein zfBcl-xL can block betanodavirus protein α-induced mitochondria-mediated secondary necrosis cell death
Authors: Horng-Cherng Wu;Chuan-Sheng Chiu;Jen-Leih Wu;Hong-Yi Gong;Ming-Chyuan Chen;Ming-Wei Lu;Jiann-Ruey Hong
Contributors: NTOU:Department of Aquaculture
Keywords: Nervous necrosis virus;Protein α;Mitochondria;zfBcl-xL;Apoptosis;Secondary necrosis cell death
Date: 2008-04
Issue Date: 2011-10-21T02:19:05Z
Publisher: Fish and Shellfish Immunology
Abstract: Abstract:Betanodavirus protein α 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 24 h post-transfection (p.t.) by Annexin V-FLUOS staining. TUNEL assay revealed apoptotic cells at 24–72 h p.t, after which post-apoptotic necrotic cells were identified by acridine orange/ethidium bromide dual dye staining from 48 to 72 h p.t. Protein α induced progressive loss of mitochondrial membrane potential (MMP) which was detected in RNA2-transfected GF-1 cells at 24, 48, and 72 h p.t., which correlated with cytochrome c release, especially at 72 h p.t. To assess the effect of zfBcl-xL on cell death, RNA2-transfected cells were co-transfected with zfBcl-xL. Co-transfection of GF-1 cells prevented loss of MMP at 24 h and 48 h p.t. and blocked initiator caspase-8 and effector caspase-3 activation at 48 h p.t. We conclude that RGNNV protein α induces apoptosis followed by secondary necrotic cell death through a mitochondria-mediated death pathway and activation of caspases-8 and -3.
Relation: 24(4), pp.436-449
URI: http://ntour.ntou.edu.tw/handle/987654321/26848
Appears in Collections:[水產養殖學系] 期刊論文

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