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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/26990

Title: Betanodavirus induces phosphatidylserine exposure and loss of mitochondrial membrane potential in secondary necrotic cells, both of which are blocked by bongkrekic acid
Authors: Shi-Ping Chen;Huey-Lang Yang;Guor Mour Her;Han-You Lin;Mei-Fen Jeng;Jen-Leih Wu;Jiann-Ruey Hong
Contributors: NTOU:Institute of Bioscience and Biotechnology
國立臺灣海洋大學:生物科技研究所
Keywords: Nervous necrosis virus;Phosphatidylserine;Mitochondria;Bongkrekic acid;Phagocytosis
Date: 2006-04-10
Issue Date: 2011-10-21T02:22:12Z
Publisher: Virology
Abstract: Abstract:In this study, we show how the red spotted grouper nervous necrosis virus (RGNNV) causes loss of mitochondrial membrane potential and promotes host secondary apoptotic necrosis. RGNNV viral proteins such as protein α (42 kDa) and protein A (110 kDa) were quickly expressed between 12 h and 24 h postinfection (p.i.) in GL-av cells. Annexin V staining revealed that the NNV infection of GL-av cells induced phosphatidylserine (PS) externalization and development of bulb-like vesicles (bleb formation) at 24 h p.i. NNV infection also induced DNA fragmentation detectable by TUNEL assay between 12 h (8%) and 72 h (32%) p.i. Bongkrekic acid (1.6 μM; BKA) blocked permeability of the mitochondrial permeability transition pore, but cyclosporine A (CsA) did not block secondary necrosis. Finally, secondary necrotic cells were not engulfed by neighboring cells. Our data suggest that RGNNV induces apoptotic death via opening the mitochondrial permeability transition pore thereby triggering secondary necrosis in the mid-apoptotic phase.
Relation: 347(2), pp.379–391
URI: http://ntour.ntou.edu.tw/handle/987654321/26990
Appears in Collections:[生命科學暨生物科技學系] 期刊論文

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