Accelerated axon loss in MOG35-55 experimental autoimmune encephalomyelitis (EAE) in myelin-associated glycoprotein-deficient (MAGKO) mice

J Neuroimmunol. 2013 Sep 15;262(1-2):53-61. doi: 10.1016/j.jneuroim.2013.06.008. Epub 2013 Jul 27.

Abstract

Myelin-associated glycoprotein (MAG) expressed by oligodendrocytes promotes the stability of axons but also impedes neural repair by inhibiting axon extension through lesioned white matter. We previously reported exacerbated axon losses in MAGKO as compared to wild type mice, 30days into experimental autoimmune encephalitis (EAE). Here, we report the time course of axon losses in EAE and show this occurs as early as 7days post-immunization, confirming MAG is protective against immune-mediated axon transection events. MAGKO mice also exhibit increased microglial activation prior to EAE, which is not seen in B4galnt1KO mice that also have axon loss, suggesting that the microglial activation may be a consequence of the loss of MAG inhibitory influence, and not a simple result of axonal degeneration.

Keywords: B4galnt1KO; EAE; MAG; Microglia; T cell; Timeline.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Axons / pathology*
  • Disease Models, Animal
  • Encephalomyelitis, Autoimmune, Experimental / chemically induced
  • Encephalomyelitis, Autoimmune, Experimental / genetics
  • Encephalomyelitis, Autoimmune, Experimental / pathology*
  • Female
  • Male
  • Mice
  • Mice, Congenic
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microglia / metabolism*
  • Microglia / pathology
  • Myelin-Associated Glycoprotein / deficiency*
  • Time Factors

Substances

  • Myelin-Associated Glycoprotein