Aquatic birnavirus infection activates the transcription factor NF-κB via tyrosine kinase signalling leading to cell death

Jiann-Ruey Hong, B. J. Guan, G. M. Her, O. Evensen, N. Santi, J. L. Wu

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Our previous studies found that infectious pancreatic necrosis virus (IPNV) induces host apoptotic cell death, possibly through a newly synthesized protein trigger. Here, we examine whether IPNV infection can induce NF-κB activation through tyrosine kinase signalling of CHSE-214 cell death (host cell death). Using the electrophoretic mobility shift assay (EMSA) to detect transcription factor activation, we found that NF-κB is apparently activated 6-8 h post-IPNV infection. Using genistein (100 μg mL-1; a tyrosine kinase inhibitor) to determine whether NF-κB activation requires tyrosine kinase activation, we found genistein blocks NF-κB activation at 8 h post-infection (p.i), and either enhances cell viability up to 50% at 12 h p.i. or blocks DNA fragmentation at 24 h p.i. Furthermore, the proteasome inhibitors PSI-I and PSI-II (both at 40 μm) also effectively blocked the NF-κB activation as well as stimulating a 30% increase in cell viability (30% decrease in apoptosis) at 8 and 12 h p.i. Taken together our data suggest that IPNV may induce NF-κB activation through tyrosine kinase signalling, which may be associated with induction of apoptosis.

Original languageEnglish
Pages (from-to)451-460
Number of pages10
JournalJournal of Fish Diseases
Volume31
Issue number6
DOIs
Publication statusPublished - 2008 Jun 1

Fingerprint

Infectious pancreatic necrosis virus
Birnaviridae
Protein-Tyrosine Kinases
tyrosine
cell death
phosphotransferases (kinases)
Cell Death
Transcription Factors
transcription factors
Genistein
virus
Virus Diseases
Infection
infection
Cell Survival
apoptosis
genistein
Apoptosis
cell viability
inhibitor

All Science Journal Classification (ASJC) codes

  • Aquatic Science
  • veterinary (miscalleneous)

Cite this

Hong, Jiann-Ruey ; Guan, B. J. ; Her, G. M. ; Evensen, O. ; Santi, N. ; Wu, J. L. / Aquatic birnavirus infection activates the transcription factor NF-κB via tyrosine kinase signalling leading to cell death. In: Journal of Fish Diseases. 2008 ; Vol. 31, No. 6. pp. 451-460.
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abstract = "Our previous studies found that infectious pancreatic necrosis virus (IPNV) induces host apoptotic cell death, possibly through a newly synthesized protein trigger. Here, we examine whether IPNV infection can induce NF-κB activation through tyrosine kinase signalling of CHSE-214 cell death (host cell death). Using the electrophoretic mobility shift assay (EMSA) to detect transcription factor activation, we found that NF-κB is apparently activated 6-8 h post-IPNV infection. Using genistein (100 μg mL-1; a tyrosine kinase inhibitor) to determine whether NF-κB activation requires tyrosine kinase activation, we found genistein blocks NF-κB activation at 8 h post-infection (p.i), and either enhances cell viability up to 50{\%} at 12 h p.i. or blocks DNA fragmentation at 24 h p.i. Furthermore, the proteasome inhibitors PSI-I and PSI-II (both at 40 μm) also effectively blocked the NF-κB activation as well as stimulating a 30{\%} increase in cell viability (30{\%} decrease in apoptosis) at 8 and 12 h p.i. Taken together our data suggest that IPNV may induce NF-κB activation through tyrosine kinase signalling, which may be associated with induction of apoptosis.",
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Aquatic birnavirus infection activates the transcription factor NF-κB via tyrosine kinase signalling leading to cell death. / Hong, Jiann-Ruey; Guan, B. J.; Her, G. M.; Evensen, O.; Santi, N.; Wu, J. L.

In: Journal of Fish Diseases, Vol. 31, No. 6, 01.06.2008, p. 451-460.

Research output: Contribution to journalArticle

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