ZFIN ID: ZDB-PUB-110920-3
Zebrafish anti-apoptotic gene Bcl-xL can prevent aquatic birnavirus-induced cell death in fish cells without affecting expression of viral proteins
Huang, H.L., Liu, Y.T., Chen, M.C., Wu, J.L., and Hong, J.R.
Date: 2011
Source: Fish & shellfish immunology   31(6): 970-7 (Journal)
Registered Authors: Hong, Jiann-Ruey, Wu, Jen-Leih
Keywords: infectious pancreatic necrosis virus, anti-apoptotic protein Bcl-xL, mitochondria membrane potential (MMP) loss, caspase-9, cell death
MeSH Terms:
  • Animals
  • Birnaviridae Infections/immunology
  • Birnaviridae Infections/veterinary*
  • Blotting, Western
  • Caspase 9/metabolism
  • Cell Death/drug effects*
  • Cell Death/immunology
  • Cell Line
  • Fish Diseases/immunology*
  • Fish Diseases/virology*
  • Green Fluorescent Proteins/metabolism
  • Matrix Metalloproteinases/metabolism
  • Membrane Potential, Mitochondrial/drug effects
  • Microscopy, Fluorescence
  • Salmon
  • Zebrafish/genetics*
  • bcl-X Protein/genetics
  • bcl-X Protein/pharmacology*
PubMed: 21906684 Full text @ Fish Shellfish Immunol.
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 (”Δψm), 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.
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