Activation of c-Jun N-terminal kinase by Akabane virus is required for apoptosis

Res Vet Sci. 2016 Aug;107:147-151. doi: 10.1016/j.rvsc.2016.06.007. Epub 2016 Jun 14.

Abstract

Akabane virus (AKAV) belongs to the Simbu serogroup of the genus Orthobunyavirus in the family Bunyaviridae. It has been shown that AKAV induces apoptosis in mammalian cells. It is necessary to understand the signaling pathways involved in AKAV-induced apoptosis to further elucidate the molecular virology of AKAV. c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) are mediators of apoptosis; therefore, we investigated the roles of JNK and p38 MAPK cascades in AKAV-infected cells. We found that JNK and p38 MAPK as well as their downstream substrates, c-Jun and heat shock protein 27 (HSP27), were phosphorylated in response to AKAV infection. A JNK inhibitor (SP600125) inhibited AKAV-mediated apoptosis whereas a p38 MAPK inhibitor (SB203580) did not. We conclude that AKAV infection activates the JNK and p38 MAPK signaling pathways, and the JNK cascade plays a crucial role in AKAV-induced apoptosis in vitro.

Keywords: Akabane virus; Apoptosis; Mitogen-activated protein kinase (MAPK).

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Chlorocebus aethiops
  • Enzyme Activation / physiology*
  • Imidazoles / pharmacology
  • JNK Mitogen-Activated Protein Kinases / genetics
  • JNK Mitogen-Activated Protein Kinases / metabolism*
  • MAP Kinase Signaling System
  • Orthobunyavirus / physiology*
  • Phosphorylation
  • Pyridines / pharmacology
  • Signal Transduction
  • Vero Cells
  • p38 Mitogen-Activated Protein Kinases / genetics
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Imidazoles
  • Pyridines
  • JNK Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • SB 203580