Zebrafish anti-apoptotic gene Bcl-xL can prevent aquatic birnavirus-induced cell death in fish cells without affecting expression of viral proteins

Hui Ling Huang, Yen Ting Liu, Ming Chyuan Chen, Jen Leih Wu, Jiann Ruey Hong

Research output: Contribution to journalArticle

Abstract

The aquatic birnavirus induces mitochondria-mediated cell death in fish; however, the molecular mechanism remains unknown. In the present study, we demonstrated that aquatic birnavirus-induced mitochondria-mediated cell death is regulated by the anti-apoptotic Bcl-2 family member, zfBcl-xL, which is anti-apoptotic and enhances host cell viability. First, CHSE-214 cells carrying EGFP-zfBcl-xL fused genes were selected, established in culture, and used to examine the involvement of zfBcl-xL in host cell protection from the effects of viral infection. EGFP-zfBcl-xL was found to prevent infectious pancreatic necrosis virus (IPNV)-induced phosphatidylserine exposure up to 40% at 12 h and 24 h post-infection (p.i.), block IPNV-induced loss of mitochondrial membrane potential (Δ. Ψm), and enhance host viability at the middle and late replication stages. In addition, zfBcl-xL overexpression prevented IPNV-induced caspase-9 activation up to 25% and 85% at the middle (12 h p.i.) and late (24 h p.i.) replication stages without affecting expression of viral proteins such as VP3 (as a viral death protein) protein. In the present study, we demonstrated that aquatic birnavirus-induced cell death is prevented by the anti-apoptotic Bcl-2 family member, zfBcl-xL, which enhances host cell viability through blockage of mitochondrial disruption and caspase-9 activation.

Original languageEnglish
Pages (from-to)970-977
Number of pages8
JournalFish and Shellfish Immunology
Volume31
Issue number6
DOIs
Publication statusPublished - 2011 Dec

All Science Journal Classification (ASJC) codes

  • Environmental Chemistry
  • Aquatic Science

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