Genetic deletion of c-Jun amino-terminal kinase 3 (JNK3) modestly increases disease severity in a mouse model of multiple sclerosis

J Neuroimmunol. 2023 Sep 15:382:578152. doi: 10.1016/j.jneuroim.2023.578152. Epub 2023 Jul 12.

Abstract

The c-Jun amino terminal kinases (JNKs) regulate transcription, and studies suggest they contribute to neuropathology in the EAE model of MS. To examine the role of the JNK3 isoform, we compared EAE in JNK3 null mice to wild type (WT) littermates. Although disease severity was similar in female mice, in male JNK3 null mice the day of onset and time to reach 100% incidence occurred sooner, and disease severity was increased. While glial activation in spinal cord was similar, white matter lesions were increased in JNK3 null mice. These results suggest JNK3 normally limits EAE disease in a sex-dependent manner.

Keywords: Astrocytes; EAE; JNK3; Microglia; Multiple sclerosis; Spinal cord.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Female
  • JNK Mitogen-Activated Protein Kinases / genetics
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Male
  • Mice
  • Mitogen-Activated Protein Kinase 10* / genetics
  • Mitogen-Activated Protein Kinase 10* / metabolism
  • Multiple Sclerosis* / genetics
  • Multiple Sclerosis* / metabolism
  • Patient Acuity
  • Phosphorylation
  • Sex Factors

Substances

  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase 10